Comprehensive Physiology Wiley Online Library
For Librarians For Authors Editors About

Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis

John H. Laragh, Jean E. Sealey

10.1002/cphy.cp080231

Source: Supplement 25: Handbook of Physiology, Renal Physiology

Originally published: 1992

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Historical Background
1.1 Renin
1.2 Aldosterone
1.3 A Coordinated Renal‐Adrenal Hormonal System: Renin, Angiotensin, and Aldosterone
2 Comparative Aspects
3 Brief Overview of the Renin‐Angiotensin‐Aldosterone System
4 Biochemistry and Molecular Biology of the Renin System
4.1 Prorenin
4.2 Renin
4.3 Renin Substrate
4.4 Angiotensins I and II
4.5 Angiotensin‐Converting Enzyme
4.6 Aldosterone
4.7 Methods of Measurement
5 Physiology
5.1 Prorenin
5.2 Renin
5.3 Renin Substrate
5.4 Angiotensin II
5.5 Aldosterone
6 Cybernetics of the System
6.1 Coordinated Regulation of Sodium, Potassium, and Blood Pressure
7 Use of the Renin System to Understand Blood Pressure Control and Disorders of Pressure‐Volume Homeostasis
7.1 Two Forms of Vasoconstriction: Vasoconstriction‐Volume Analysis
7.2 Three Basic Tenets Concerning Plasma Renin Measurements
7.3 The Sodium—Calcium Connection
7.4 Dynamic Reciprocity of Two Forms of Vasoconstriction
7.5 The Sympathetic Nervous System and Modulation of the Two Forms of Arteriolar Vasoconstriction
8 Human Disorders of the Renin System
8.1 Hypertensive Disorders
8.2 Renin System Abnormalities in Edematous States
8.3 Hypokalemic Normotensive States
9 Summary
Figure 1. Figure 1.

Renin‐angiotensin‐aldosterone system. Renin, secreted in response to reduced arterial pressure or reduced renal tubular sodium, cleaves angiotensin I from circulating angiotensinogen (renin substrate). Angiotensin‐converting enzyme (ACE) then converts angiotensin I to angiotensin II. Angiotensin II raises pressure by direct arteriolar vasoconstriction and stimulates adrenal aldosterone secretion; together, aldosterone and angiotensin II cause renal sodium retention. Resultant fluid accumulation leads to improved flow. These pressure and volume effects in turn lead to suppression of renin release. Dashed line indicates negative feedback.

From Laragh et al. 537
Figure 2. Figure 2.

Amino acid sequence of human preprorenin. Asp38 and Asp226 are the two aspartic acids involved in catalysis. Large arrows are likely sites of hydrolysis of signal peptide and prosequence.

From Morris et al. 641
Figure 3. Figure 3.

Relation of renin activity in plasma samples obtained at noon, and of corresponding 24 h urinary excretion of aldosterone, to concurrent daily rate of sodium excretion. For these normal subjects, data describe dynamic hyperbolic relationship between each hormone and sodium excretion. Dynamic fluctuations in renin in response to changes in sodium intake help to maintain blood pressure constant during wide changes in sodium balance. Renin and aldosterone responses work together in kidney to conserve or eliminate sodium in response to changes in dietary sodium intake. Of note is that subjects studied on random diets outside the hospital or while on carefully controlled diets in the hospital exhibited similar relationships–a finding that validates use of this nomogram in studying outpatients or subjects not receiving constant diets.

Laragh et al. 527
Figure 4. Figure 4.

Relationship of renal vein renin to arterial renin in patients with essential hypertension. (Peripheral venous, infrarenal inferior vena caval, and arterial renin levels are identical and interchangeable in this relationship.) Dashed line is described by loge renal vein renin = 1.24 + 1.02 loge arterial renin. Slope of the line is not different from line of identity, indicating that relationship of renal vein renin to arterial renin is constant at all levels of plasma renin activity found in essential hypertension. Intercept of 1.24 indicates that renal vein renin is 124% of arterial renin. AI, angiotensin I.

From Sealey et al. 828
Figure 5. Figure 5.

Equations illustrating how renal plasma flow can be roughly calculated in human subjects from renal vein renin (V) and peripheral venous, infrarenal inferior vena caval, or arterial (A) renin measurements. Equations are especially useful in diagnosis of unilateral renovascular hypertension when renin is secreted from only one kidney (see later under Renovascular Hypertension).

From Sealey et al. 828
Figure 6. Figure 6.

Response of arterial blood pressure (BP) to intravenous injection (arrow) of renin (R) and angiotensin (A). It can be seen in an animal model that pressor response to renin is delayed and prolonged relative to that of angiotensin because it is a consequence of enzymatic generation of angiotensin II, which has immediate and short‐lived pressor action.

Lee et al. 560
Figure 7. Figure 7.

Effect of differences in renin substrate concentration on rate of generation of angiotensin. There was no difference in rate when undiluted plasma samples exhibiting various angiotensinogen concentrations were compared with various dilutions of plasma that had endogenously high renin substrate. These samples were obtained at various times during oral contraceptive administration. Normal substrate concentration is ∼1,800 ng/ml. Data suggest that concentration of angiotensinogen in human plasma is normally rate limiting. They also suggest that observed differences in rate of angiotensin generation are related to differences in renin substrate concentration and not to variations in concentration of activator or inhibitor of renin.

From Newton et al. 676
Figure 8. Figure 8.

Steps in processing and degradation of angiotensin. Converting enzyme activity probably occurs primarily in pulmonary circulation, but is also present on vascular endothelial cells and in blood.

From Gocke et al. 348
Figure 9. Figure 9.

Biosynthetic pathways from cholesterol to mineralocorticoids (aldosterone), glucocorticoids (cortisol), and androgens (androstenedione) are shown, as are structures of cholesterol, aldosterone, cortisol, and androstenedione (small amounts of testosterone and estrogen are also synthesized in adrenal gland). Positions 3, 11, 17, 18, and 21 are marked on diagram of a steroid molecule (bottom right), Arrows indicate individual biosynthetic conversions. Enzyme specifically mediating each step is indicated at top or left, with name of enzymatic activity in parentheses; note that one protein can mediate more than one step. OH hydroxyl and CMO corticosterone methyl oxidase.

From White et al. 971
Figure 10. Figure 10.

Relationship, on log‐log scale, of 24 h urine potassium excretion to 24 h excretion of acidlabile conjugate of aldosterone. Data are from longitudinal study of 254 normal subjects evaluated once a year for 4–9 years. Each point represents data from randomly collected urine sample. Ranges of sodium and potassium excretions reflect normal differences in dietary habits, except that in 1 year 144 of the subjects were asked to restrict their sodium intake moderately. Panels reflect three different ranges of sodium. Relationships between urine potassium and urine aldosterone are described by equations log aldo = 1.21 log UKV‐1.17 (UNaV<80), R = 0.70, P<.001; log aldo = 0.89 log UKV‐0.76 (UNaV 80–150) R = 0.55, P<.001; log aldo = 0.69 log UKV‐0.52 (UNaV>150 mEq/day), R = 0.45, P<.001.

From James et al., unpublished data
Figure 11. Figure 11.

Relationship between plasma active renin and proportion of plasma inactive renin (prorenin). Large circles labeled A, B, and C represent three patients with ectopic renin‐secreting tumors. Small closed circles represent normal subjects; open symbols, essential hypertensive patients with low (□), normal (○), or high (Δ) renin‐sodium profiles. ▪, Primary aldosteronism; ▴, malignant or renovascular hypertension; a, adrenal cortical insufficiency; b, Bartter's syndrome; c, hepatic cirrhosis; g, ganglioneuroma; t, trophoblastic disease. Absolute levels of renin and prorenin in these patients are published in Atlas et al. 24.

From Atlas et al. 24
Figure 12. Figure 12.

Hormonal changes throughout menstrual cycle in one normal woman. Day zero = LH (luteinizing hormone) peak; FSH, follicle‐stimulating hormone. Note that peak of prorenin immediately follows LH surge and is not accompanied by change in active renin.

From Sealey et al. 829
Figure 13. Figure 13.

Juxtaglomerular apparatus of rat, illustrating tubular and vascular components. Tubular component consists of specialized region of thick ascending limb of Henle–macula densa (MD). This can be identified by close proximity of nuclei of these cells to each other. Vascular component consists of afferent (A) and efferent (E) arterioles and extraglomerular mesangium (EM; also known as “lacis,” “group of cells of Goormaghtigh,” and “polkissen”). MD is in contact with EM. EM is continuous with intraglomerular mesangium (IM). Granular cells (GC) are seen in walls of glomerular arterioles and are most abundant in afferent arteriole, but positive cells can occur in IM and efferent arterioles. Vascular and tubular components are innervated by sympathetic nerves (N). B, Bowman's space; G, glomerular capillary.

From Barajas 41
Figure 14. Figure 14.

Hypothetical renin‐containing juxtaglomerular cell plasma membrane. Sodium–calcium exchange carrier binds Na+ and Ca2+ in 3:1 ratio. In presence of normal transmembrane Na+ electrochemical gradient, Na+ influx down its gradient is coupled with Ca2+ efflux against its gradient; decreases in Na+ electrochemical gradient (caused by membrane depolarization, increased , or decreased ) decrease rate of Ca2+ efflux and conversely. Transmembrane Na+ and K+ concentration gradients, and ultimately transmembrane potential, are maintained by primary active transport of Na+ and K+ (Na+,K+‐ATPase).

From Churchill 191
Figure 15. Figure 15.

Time course of renin release from single perfused juxtaglomerular apparatus (JGA). Top: time course of renin secretion from six JGA perfused with control solution throughout experiments. After 50 min a mock perfusate change was made. Bottom: time course of renin secretion from six JGA perfused with control solution for initial 50 min (closed circles), after which perfusate was changed to low NaCl isosmotic solution (open circles). Values given are arithmetic means; bars show SEM. In upper panel, mean renin release rate did not differ between control and experimental periods, whereas in lower panel a significant increase occurred in the experimental period relative to control (P<0.01, paired t test). Asterisks indicate P values for comparison of individual time periods with corresponding periods in time control series (*P<0.05, **P<0.02).

From Skøtt and Briggs 866
Figure 16. Figure 16.

Effect of 30 min of 65° head‐up tilt in normal subjects before and after 0.12 mg/kg intravenous propranolol HCI during high sodium (200 mEq/day) and low sodium (10 mEq/day) intakes. When renin increase in response to tilt was blocked by propranolol during high sodium intake, blood pressure was not compromised (left panel). This was in contrast to effect on low sodium intake where the baseline renin was higher and response of renin to tilt was greater (right panel). When this response was blocked by propranolol, blood pressure fell dramatically. This study illustrates importance of renin system in maintaining blood pressure during sodium depletion and upright posture.

From Morganti et al. 638
Figure 17. Figure 17.

Hormonal changes in one young woman during two 24 h periods separated by 1 week. Dietary intake on each day was 100 mEq/day sodium, 60 mEq/day potassium. Left: subject was supine for 23 h, from 9 A.M. to 8 A.M. the following day. Right: subject went about her daily work and was supine only from 11 P.M. to 8 A.M. During continuously supine day, atrial natriuretic factor (ANF) increased at start of bed rest and then gradually fell, reaching its lowest level from 9 P.M. to 3 A.M. It rose again between 6 and 8 A.M. There was no apparent effect of ANF on aldosterone to renin relationships (UA/PRA). During ambulatory/supine study, lowest aldosterone levels and lowest UA/PRA ratio occurred when ANF increased to >20 fmol/ml, which occurred between 12 P.M. and 6 A.M. This would be consistent with well‐known effects of ANF in vitro to suppress aldosterone response to angiotensin II stimulation. (From Bell et al., unpublished data.)
Figure 18. Figure 18.

Blood (black areas) and plasma (dotted areas) volumes, cumulative sodium balance, plasma renin activity, and daily urinary aldosterone excretion data for six normal subjects on I, normal sodium intake; IV, after sodium depletion and consequent blood volume reduction; V, during sodium repletion without volume repletion; and VI, during volume repletion without concurrent increase in sodium balance. Volume expansion was prevented during period V by serial bleedings. Plasma renin activity fell during sodium repletion (period V) despite fall in total blood volume in all subjects. Renin therefore appears to respond to sodium and not to total blood volume.

From Bull et al. 137
Figure 19. Figure 19.

Prolonged continuous angiotensin infusion in normal subject for 11 days. Dose of angiotensin was adjusted to maintain mildly pressor response. Angiotensin II induced marked and selective increase in adrenal cortical secretion of aldosterone. Together with direct effect of angiotensin II on proximal tubule sodium reabsorption, rise in aldosterone caused sodium retention. As sodium was retained, angiotensin became more pressor. Because of this increasing pressor sensitivity to angiotensin, dose of angiotensin II had to be serially reduced to maintain same level of blood pressure. Consequently, aldosterone secretion fell to close to control levels. Thus pressor sensitivity to angiotensin increased as sodium retention progressed. Results indicate angiotensin, unlike norepinephrine, can produce and then sustain hypertension in progressively smaller amounts as sodium‐volume gain turns off need for angiotensin.

From Laragh et al. 547
Figure 20. Figure 20.

Effect of angiotensin II on aldosterone secretion in eight normal subjects. In all eight experiments infusion of angiotensin II caused significant increase in adrenal secretory rate of aldosterone as compared with control infusion of isotonic glucose. Urinary sodium excretion usually decreased with angiotensin, a finding consistent with increased aldosterone production and a direct renal effect of angiotensin II.

From Laragh et al. 525
Figure 21. Figure 21.

Study of effect of increased potassium administration for 5 days in normal subject maintained on constant dietary sodium regimen. Plasma renin activity (PRA) was serially suppressed as urinary aldosterone and urinary sodium and potassium increased. Closed circles are plasma Na+ and plasma K+.

From Brunner et al. 123
Figure 22. Figure 22.

Effect of potassium administration on aldosterone secretion of two patients with renal tubule disease. Large changes in aldosterone secretion rate occurred in response to increased potassium intake (solid bars) when patients received normal sodium diet. Potassium administration during sodium depletion induced even greater hypersecretion of aldosterone. In both studies serum potassium concentration increased but did not exceed normal levels.

From Cannon et al. 153
Figure 23. Figure 23.

Effect of intramuscular administration of ACTH, 40 U b.i.d., in normal subject. ACTH increased aldosterone excretion much more during sodium depletion (left) than during normal sodium intake (right). However, response to ACTH was not sustained during 5 days of administration on either sodium intake, and aldosterone actually fell below baseline levels when injections were terminated during sodium deprivation and while ACTH was administered during normal sodium intake.

From Newton and Laragh 675
Figure 24. Figure 24.

Renin system in normal subjects divided according to blood pressure and plasma renin levels. Analysis was carried out in 139 normal subjects divided into normotensive [n = 99, solid boxes and lines; diastolic blood pressure (DBP) < 85 mm Hg] and borderline hypertensive groups (n = 40, dashed boxes and lines; DBP 85–100 mm Hg). Each blood pressure group was subdivided on basis of renin level into low (<1 ng/ml/h, n = 14, 7), medium (1–5 ng/ml/h, n = 77, 26), or high (>5 ng/ml/h, n = 8, 7) renin groups. As expected, urine and plasma aldosterone followed renin levels. Nonetheless, differences in aldosterone between groups were not as great on a percentage basis; nor were they always statistically significant. Urine aldosterone to renin ratio (UA/PRA) was highest in both low renin groups and lowest in both high renin groups. This could not be ascribed to effect of potassium to stimulate aldosterone, because low renin groups did not have higher urine or serum potassium. Low renin subjects seem to have increased adrenal sensitivity to angiotensin II, but basis for this is unexplained.

From Sealey et al., unpublished data
Figure 25. Figure 25.

Illustration of link between sodium balance and blood pressure homeostasis and between sodium balance and potassium homeostasis. However, there is little evidence for link between potassium and blood pressure.
Figure 26. Figure 26.

Data from Figure 3 replotted to illustrate mean urinary sodium excretion for given ranges of plasma renin activity and urinary aldosterone excretion. Differences in sodium excretion are significant at all higher rates suggesting that angiotensin and aldosterone continue to exert regulatory effect on urinary sodium excretion even when circulating concentrations are low.

From Laragh et al. 544
Figure 27. Figure 27.

Periodic fluctuations in urine sodium excretion, sodium balance, plasma renin activity, and urine aldosterone excretion after initiation of high sodium diet (270 mEq), which was preceded by 11 days of sodium deprivation (10 mEq/day) (not shown here; see Fig. 30). Mean values ±SD from three normal subjects are presented. Each subject exhibited similar periodic fluctuation in urine sodium, renin, and aldosterone. After 4 days of diet, natriuresis occurred for 3 days, and these high levels of sodium excretion were associated with lowest levels of plasma renin activity and aldosterone excretion.

From Sealey et al. 827
Figure 28. Figure 28.

Demonstration that when angiotensin II is fixed during changes in sodium intake, blood pressure increases with sodium loading and is at its lowest level with sodium depletion. Changes in mean arterial pressure during chronic changes in sodium intake in control dogs and in dogs during angiotensin II blockade with the converting enzyme inhibitor SQ 14.225 or during angiotensin II infusion (5 mg‐kg−1.min) also shown. Values are means ±SE.

From Hall et al. 380
Figure 29. Figure 29.

Top: interrelationship of renin‐aldosterone hormonal system with changes in sodium and potassium balance. Bottom: coordination of intrarenal physical factors with hormonal factors for sodium and potassium homeostasis. Rate of excretion of each cation is determined by interaction of aldosterone with distal tubular sodium supply.

From Sealey and Laragh 838
Figure 30. Figure 30.

Effect of sodium depletion on urine aldosterone excretion and potassium balance–combined results from five normal subjects. Despite hyperaldosteronism induced by sodium depletion, potassium balance became progressively positive. Therefore, other factors (see Fig. 29) counterbalance kaliuretic action of aldosterone. Increase in aldosterone‐renin ratio most likely reflects gradual increase in potassium balance; this change was accompanied by only modest increases in plasma potassium.

From Laragh et al. 543
Figure 31. Figure 31.

Acute effects (at 90 min) of two different converting enzyme inhibitors, teprotide and captopril, on diastolic blood pressure. With both drugs, percent fall in blood pressure is closely related to pretreatment levels of plasma renin activity in quietly seated, untreated hypertensive patients. Note also that almost every subject exhibited some hypotensive response to drug, again illustrating (see Fig. 26) that even low levels of renin may have an effect. Left: effects of administering nonapeptide (isolated from snake venom) teprotide (SQ 20881), intravenously to 89 patients; data are replotted from Case et al. 173,175. Right: changes in seated diastolic blood pressure 90 min after single oral dose of 25 mg captopril to 166 patients; data are replotted from Case et al. 172 and Laragh et al. 532. Setting aside errors in cuff pressure measurements, data reveal remarkable and extremely similar correlations between height of pretreatment plasma renin value and degree of induced decrease in blood pressure. Note that patients with plasma renin values <1.0 ng/ml/h exhibited smallest change in pressure. Both sets of data also provide strong indirect evidence that plasma renin value reflects active role of renin in supporting arterial pressure in hypertensive persons.

Data replotted from Case et al. 172,173,175 and Laragh et al. 532
Figure 32. Figure 32.

Relationship between acute (60 min) fall in diastolic pressure and baseline renin in response to oral captopril (25–50 mg) in group of hypertensive patients divided into those with 30 min seated renins of <1, 1–6, or >6 ng/ml/h. The higher the baseline renin of each group, the greater the fall in diastolic pressure. On average, captopril lowered diastolic pressure by close to 20 mm Hg in the 74 high renin patients; fall was only 5 mm Hg in low renin group.

From Mueller et al. 647
Figure 33. Figure 33.

Serum levels of magnesium (left) and ionized calcium (right) in normotensive control subjects (N1 BP) and in different renin subgroups of essential hypertensive subjects. Low, medium, and high renin essential hypertension abbreviated as Lo RH, N1 RH, and Hi RH, respectively. For both cations, hypertensive patients differ significantly from normotensive controls. To convert to millimoles per liter, multiply by 0.5.

From Resnick et al. 776
Figure 34. Figure 34.

Relationship of the percent fall in systolic pressure during treatment with verapamil (120 mg, 3xday) to baseline ambulatory plasma renin activity in 13 hypertensive patients. Patients represented by circles were on low‐sodium intake (9 mEq/day); those represented by triangles were on a high‐sodium intake (212 mEq/day). Those on high‐sodium intake and those with lower plasma renin levels were more responsive to the calcium channel blocker.

From Nicholson et al. 681
Figure 35. Figure 35.

Cellular calcium hypothesis of hypertension that reconciles observed heterogeneous extracellular divalent cation levels among hypertensive patients with their presumed uniformly abnormal intracellular concentrations, ex, Extracellular calcium; cyt, cytosolic free calcium; BP, blood pressure.

From Resnick 772
Figure 36. Figure 36.

In two‐kidney, one‐clip renal hypertensive rats infusion of angiotensin receptor antagonist saralasin induced immediate fall in blood pressure, which reached −40.8±4.2 mm Hg after 60 min (P<0.001). In contrast, change in blood pressure induced in one‐kidney, one‐clip renal hypertensive rats was not significant (P>0.1).

From Brunner et al. 126
Figure 37. Figure 37.

In sodium‐depleted, one‐kidney, one‐clip renovascular hypertensive rats, infusion of angiotensin II antagonist saralasin produced striking falls in blood pressure. Twenty‐four hours later, after same animals were sodium repleted, there was no significant effect on blood pressure by same dose of antagonist. These studies illustrate dynamic relationship between sodium and renin in maintaining elevated blood pressure of this form of renovascular hypertension

From Gavras et al. 338
Figure 38. Figure 38.

Illustration that blood pressure reduction induced by angiotensin II blockade can be reversed by sodium loading in patient with malignant hypertension (studied under balance ward conditions). First vasoconstriction and then volume support to hypertension are shown. Angiotensin blockade with saralasin produced dramatic fall in blood pressure. However, as blockade was maintained, when sodium chloride was infused over next 40 h, blood pressure returned to high control values and excess volume replaced vasoconstriction in support of blood pressure. Administration of 40 mg Lasix (L40) during continued angiotensin II blockade resulted in diuresis and fall in blood pressure.

From Brunner et al. 125
Figure 39. Figure 39.

Metabolism balance study of patient with pseudoprimary aldosteronism. Dotted lines indicate intakes of potassium and sodium. Normal ranges for aldosterone secretion and for midday serum renin in ambient subjects for each dietary sodium intake are indicated by range bars. Aldosterone secretion was always markedly elevated, and serum renin levels were abnormally low. Responses of aldosterone and renin to manipulations in sodium intake were blunted. Potassium repletion was more easily accomplished when dietary sodium was reduced.

From Ledingham et al. 535
Figure 40. Figure 40.

Renal–adrenal axis is hormonal cascade involving renin, angiotensin, and aldosterone for regulation of sodium and potassium balance and blood pressure. Interaction is depicted as it was first discovered in studies of patients with malignant hypertension in whom, because of defective feedback, it is involved in causation. Accordingly, there is massive excess of both renin and aldosterone that cannot turn itself off.

From Laragh et al. 507
Figure 41. Figure 41.

Different high blood pressure mechanisms, pathophysiological changes, and treatment strategies in high and low renin hypertensive patients.

Adapted from Laragh et al. 512
Figure 42. Figure 42.

Different blood pressure mechanisms in two animal models of renovascular (i.e., Goldblatt) hypertension. Although comparable blood pressure elevation occurs in Goldblatt hypertension of either the one‐kidney or two‐kidney type, different mechanisms are involved. Volume overexpansion from impaired renal excretory capacity is implicated in one‐kidney type, whereas renin‐initiated vasoconstriction appears largely responsible for two‐kidney type.

From Laragh et al. 545
Figure 43. Figure 43.

Dramatic difference in 60‐min plasma renin response to single oral dose of converting enzyme inhibitor captopril between patients with essential hypertension and those with renovascular disease. Response is used as basis of screening test for renovascular hypertension.

From Mueller et al. 647
Figure 44. Figure 44.

Renal angioplasty reduces plasma renin activity into normal range in patients with renovascular hypertension. Left: before angioplasty; right: 6 months after angioplasty. Hatched area shows normal range of plasma renin in relation to concurrent 24 h urine sodium excretion.

From Pickering et al. 748
Figure 45. Figure 45.

Renal vein renin diagnostic patterns. In essential hypertension (top), renin level in each renal vein is ∼25% greater than peripheral arterial, venous, or infrarenal inferior vena caval renin at all levels of renin secretion. In setting of unilateral renin secretion (curable renovascular hypertension; bottom left), affected kidney is solely responsible for maintaining peripheral renin levels. Hence, increment is at least 50% (0.5) and becomes progressively greater as renal blood flow is reduced. Patients with unilateral secretion of renin and normal BUN and'serum creatinine can usually be cured by angioplasty, surgical repair, or nephrectomy. But, if BUN and serum creatinine are elevated, bilateral disease is likely, even if contralateral suppression of renin secretion is observed. Unequal bilateral renin secretion (bottom right) indicates bilateral disease and decreases change of cure following unilateral nephrectomy, but improvement or even cure may be possible following angioplasty or corrective surgery. V1, renal vein renin; V2, renal vein renin on opposite side; IVC, inferior vena caval renin. Bold face large numbers indicate levels of plasma renin at the sites indicated.

From Laragh & Seale 541
Figure 46. Figure 46.

Relation of noon ambulatory plasma renin activity (left) and corresponding daily urinary aldosterone excretion (right) to concurrent daily rate of urinary sodium excretion. Dashed lines outline normal channel derived from study of normotensive people (see Fig. 3). Total of 219 patients with untreated essential hypertension were studied, some on several occasions and at different levels of sodium intake. Three major subgroups (▴, low renin, ○, normal renin, and ▪, high renin essential hypertension) are defined by appropriateness or normalcy of plasma renin activity to rate of sodium excretion, used as index of dietary intake. Additional abnormal subgroups are defined when aldosterone (right) is included in the analysis.

From Brunner et al. 127
Figure 47. Figure 47.

Response to intravenous converting enzyme inhibition (MK 422) based on specific mechanisms of vasoconstriction. Left: High renin heart failure patient has prompt hemodynamic improvement following small dose of intravenous enalaprilat with further improvement in repeat challenge. Right: Low renin patient with comparable heart failure did not respond to intravenous enalaprilat but had prompt response to oral calcium channel inhibitor nifedipine (10 mg). Findings are representative of relative selectivity of response based on the mechanism of vasoconstriction. MAP, mean arterial pressure; PCWP, pulmonary capillary wedge pressure; CI, cardiac index; SVR, systemic vascular resistance.

From Cody et al. 196


Figure 1.

Renin‐angiotensin‐aldosterone system. Renin, secreted in response to reduced arterial pressure or reduced renal tubular sodium, cleaves angiotensin I from circulating angiotensinogen (renin substrate). Angiotensin‐converting enzyme (ACE) then converts angiotensin I to angiotensin II. Angiotensin II raises pressure by direct arteriolar vasoconstriction and stimulates adrenal aldosterone secretion; together, aldosterone and angiotensin II cause renal sodium retention. Resultant fluid accumulation leads to improved flow. These pressure and volume effects in turn lead to suppression of renin release. Dashed line indicates negative feedback.

From Laragh et al. 537


Figure 2.

Amino acid sequence of human preprorenin. Asp38 and Asp226 are the two aspartic acids involved in catalysis. Large arrows are likely sites of hydrolysis of signal peptide and prosequence.

From Morris et al. 641


Figure 3.

Relation of renin activity in plasma samples obtained at noon, and of corresponding 24 h urinary excretion of aldosterone, to concurrent daily rate of sodium excretion. For these normal subjects, data describe dynamic hyperbolic relationship between each hormone and sodium excretion. Dynamic fluctuations in renin in response to changes in sodium intake help to maintain blood pressure constant during wide changes in sodium balance. Renin and aldosterone responses work together in kidney to conserve or eliminate sodium in response to changes in dietary sodium intake. Of note is that subjects studied on random diets outside the hospital or while on carefully controlled diets in the hospital exhibited similar relationships–a finding that validates use of this nomogram in studying outpatients or subjects not receiving constant diets.

Laragh et al. 527


Figure 4.

Relationship of renal vein renin to arterial renin in patients with essential hypertension. (Peripheral venous, infrarenal inferior vena caval, and arterial renin levels are identical and interchangeable in this relationship.) Dashed line is described by loge renal vein renin = 1.24 + 1.02 loge arterial renin. Slope of the line is not different from line of identity, indicating that relationship of renal vein renin to arterial renin is constant at all levels of plasma renin activity found in essential hypertension. Intercept of 1.24 indicates that renal vein renin is 124% of arterial renin. AI, angiotensin I.

From Sealey et al. 828


Figure 5.

Equations illustrating how renal plasma flow can be roughly calculated in human subjects from renal vein renin (V) and peripheral venous, infrarenal inferior vena caval, or arterial (A) renin measurements. Equations are especially useful in diagnosis of unilateral renovascular hypertension when renin is secreted from only one kidney (see later under Renovascular Hypertension).

From Sealey et al. 828


Figure 6.

Response of arterial blood pressure (BP) to intravenous injection (arrow) of renin (R) and angiotensin (A). It can be seen in an animal model that pressor response to renin is delayed and prolonged relative to that of angiotensin because it is a consequence of enzymatic generation of angiotensin II, which has immediate and short‐lived pressor action.

Lee et al. 560


Figure 7.

Effect of differences in renin substrate concentration on rate of generation of angiotensin. There was no difference in rate when undiluted plasma samples exhibiting various angiotensinogen concentrations were compared with various dilutions of plasma that had endogenously high renin substrate. These samples were obtained at various times during oral contraceptive administration. Normal substrate concentration is ∼1,800 ng/ml. Data suggest that concentration of angiotensinogen in human plasma is normally rate limiting. They also suggest that observed differences in rate of angiotensin generation are related to differences in renin substrate concentration and not to variations in concentration of activator or inhibitor of renin.

From Newton et al. 676


Figure 8.

Steps in processing and degradation of angiotensin. Converting enzyme activity probably occurs primarily in pulmonary circulation, but is also present on vascular endothelial cells and in blood.

From Gocke et al. 348


Figure 9.

Biosynthetic pathways from cholesterol to mineralocorticoids (aldosterone), glucocorticoids (cortisol), and androgens (androstenedione) are shown, as are structures of cholesterol, aldosterone, cortisol, and androstenedione (small amounts of testosterone and estrogen are also synthesized in adrenal gland). Positions 3, 11, 17, 18, and 21 are marked on diagram of a steroid molecule (bottom right), Arrows indicate individual biosynthetic conversions. Enzyme specifically mediating each step is indicated at top or left, with name of enzymatic activity in parentheses; note that one protein can mediate more than one step. OH hydroxyl and CMO corticosterone methyl oxidase.

From White et al. 971


Figure 10.

Relationship, on log‐log scale, of 24 h urine potassium excretion to 24 h excretion of acidlabile conjugate of aldosterone. Data are from longitudinal study of 254 normal subjects evaluated once a year for 4–9 years. Each point represents data from randomly collected urine sample. Ranges of sodium and potassium excretions reflect normal differences in dietary habits, except that in 1 year 144 of the subjects were asked to restrict their sodium intake moderately. Panels reflect three different ranges of sodium. Relationships between urine potassium and urine aldosterone are described by equations log aldo = 1.21 log UKV‐1.17 (UNaV<80), R = 0.70, P<.001; log aldo = 0.89 log UKV‐0.76 (UNaV 80–150) R = 0.55, P<.001; log aldo = 0.69 log UKV‐0.52 (UNaV>150 mEq/day), R = 0.45, P<.001.

From James et al., unpublished data


Figure 11.

Relationship between plasma active renin and proportion of plasma inactive renin (prorenin). Large circles labeled A, B, and C represent three patients with ectopic renin‐secreting tumors. Small closed circles represent normal subjects; open symbols, essential hypertensive patients with low (□), normal (○), or high (Δ) renin‐sodium profiles. ▪, Primary aldosteronism; ▴, malignant or renovascular hypertension; a, adrenal cortical insufficiency; b, Bartter's syndrome; c, hepatic cirrhosis; g, ganglioneuroma; t, trophoblastic disease. Absolute levels of renin and prorenin in these patients are published in Atlas et al. 24.

From Atlas et al. 24


Figure 12.

Hormonal changes throughout menstrual cycle in one normal woman. Day zero = LH (luteinizing hormone) peak; FSH, follicle‐stimulating hormone. Note that peak of prorenin immediately follows LH surge and is not accompanied by change in active renin.

From Sealey et al. 829


Figure 13.

Juxtaglomerular apparatus of rat, illustrating tubular and vascular components. Tubular component consists of specialized region of thick ascending limb of Henle–macula densa (MD). This can be identified by close proximity of nuclei of these cells to each other. Vascular component consists of afferent (A) and efferent (E) arterioles and extraglomerular mesangium (EM; also known as “lacis,” “group of cells of Goormaghtigh,” and “polkissen”). MD is in contact with EM. EM is continuous with intraglomerular mesangium (IM). Granular cells (GC) are seen in walls of glomerular arterioles and are most abundant in afferent arteriole, but positive cells can occur in IM and efferent arterioles. Vascular and tubular components are innervated by sympathetic nerves (N). B, Bowman's space; G, glomerular capillary.

From Barajas 41


Figure 14.

Hypothetical renin‐containing juxtaglomerular cell plasma membrane. Sodium–calcium exchange carrier binds Na+ and Ca2+ in 3:1 ratio. In presence of normal transmembrane Na+ electrochemical gradient, Na+ influx down its gradient is coupled with Ca2+ efflux against its gradient; decreases in Na+ electrochemical gradient (caused by membrane depolarization, increased , or decreased ) decrease rate of Ca2+ efflux and conversely. Transmembrane Na+ and K+ concentration gradients, and ultimately transmembrane potential, are maintained by primary active transport of Na+ and K+ (Na+,K+‐ATPase).

From Churchill 191


Figure 15.

Time course of renin release from single perfused juxtaglomerular apparatus (JGA). Top: time course of renin secretion from six JGA perfused with control solution throughout experiments. After 50 min a mock perfusate change was made. Bottom: time course of renin secretion from six JGA perfused with control solution for initial 50 min (closed circles), after which perfusate was changed to low NaCl isosmotic solution (open circles). Values given are arithmetic means; bars show SEM. In upper panel, mean renin release rate did not differ between control and experimental periods, whereas in lower panel a significant increase occurred in the experimental period relative to control (P<0.01, paired t test). Asterisks indicate P values for comparison of individual time periods with corresponding periods in time control series (*P<0.05, **P<0.02).

From Skøtt and Briggs 866


Figure 16.

Effect of 30 min of 65° head‐up tilt in normal subjects before and after 0.12 mg/kg intravenous propranolol HCI during high sodium (200 mEq/day) and low sodium (10 mEq/day) intakes. When renin increase in response to tilt was blocked by propranolol during high sodium intake, blood pressure was not compromised (left panel). This was in contrast to effect on low sodium intake where the baseline renin was higher and response of renin to tilt was greater (right panel). When this response was blocked by propranolol, blood pressure fell dramatically. This study illustrates importance of renin system in maintaining blood pressure during sodium depletion and upright posture.

From Morganti et al. 638


Figure 17.

Hormonal changes in one young woman during two 24 h periods separated by 1 week. Dietary intake on each day was 100 mEq/day sodium, 60 mEq/day potassium. Left: subject was supine for 23 h, from 9 A.M. to 8 A.M. the following day. Right: subject went about her daily work and was supine only from 11 P.M. to 8 A.M. During continuously supine day, atrial natriuretic factor (ANF) increased at start of bed rest and then gradually fell, reaching its lowest level from 9 P.M. to 3 A.M. It rose again between 6 and 8 A.M. There was no apparent effect of ANF on aldosterone to renin relationships (UA/PRA). During ambulatory/supine study, lowest aldosterone levels and lowest UA/PRA ratio occurred when ANF increased to >20 fmol/ml, which occurred between 12 P.M. and 6 A.M. This would be consistent with well‐known effects of ANF in vitro to suppress aldosterone response to angiotensin II stimulation. (From Bell et al., unpublished data.)



Figure 18.

Blood (black areas) and plasma (dotted areas) volumes, cumulative sodium balance, plasma renin activity, and daily urinary aldosterone excretion data for six normal subjects on I, normal sodium intake; IV, after sodium depletion and consequent blood volume reduction; V, during sodium repletion without volume repletion; and VI, during volume repletion without concurrent increase in sodium balance. Volume expansion was prevented during period V by serial bleedings. Plasma renin activity fell during sodium repletion (period V) despite fall in total blood volume in all subjects. Renin therefore appears to respond to sodium and not to total blood volume.

From Bull et al. 137


Figure 19.

Prolonged continuous angiotensin infusion in normal subject for 11 days. Dose of angiotensin was adjusted to maintain mildly pressor response. Angiotensin II induced marked and selective increase in adrenal cortical secretion of aldosterone. Together with direct effect of angiotensin II on proximal tubule sodium reabsorption, rise in aldosterone caused sodium retention. As sodium was retained, angiotensin became more pressor. Because of this increasing pressor sensitivity to angiotensin, dose of angiotensin II had to be serially reduced to maintain same level of blood pressure. Consequently, aldosterone secretion fell to close to control levels. Thus pressor sensitivity to angiotensin increased as sodium retention progressed. Results indicate angiotensin, unlike norepinephrine, can produce and then sustain hypertension in progressively smaller amounts as sodium‐volume gain turns off need for angiotensin.

From Laragh et al. 547


Figure 20.

Effect of angiotensin II on aldosterone secretion in eight normal subjects. In all eight experiments infusion of angiotensin II caused significant increase in adrenal secretory rate of aldosterone as compared with control infusion of isotonic glucose. Urinary sodium excretion usually decreased with angiotensin, a finding consistent with increased aldosterone production and a direct renal effect of angiotensin II.

From Laragh et al. 525


Figure 21.

Study of effect of increased potassium administration for 5 days in normal subject maintained on constant dietary sodium regimen. Plasma renin activity (PRA) was serially suppressed as urinary aldosterone and urinary sodium and potassium increased. Closed circles are plasma Na+ and plasma K+.

From Brunner et al. 123


Figure 22.

Effect of potassium administration on aldosterone secretion of two patients with renal tubule disease. Large changes in aldosterone secretion rate occurred in response to increased potassium intake (solid bars) when patients received normal sodium diet. Potassium administration during sodium depletion induced even greater hypersecretion of aldosterone. In both studies serum potassium concentration increased but did not exceed normal levels.

From Cannon et al. 153


Figure 23.

Effect of intramuscular administration of ACTH, 40 U b.i.d., in normal subject. ACTH increased aldosterone excretion much more during sodium depletion (left) than during normal sodium intake (right). However, response to ACTH was not sustained during 5 days of administration on either sodium intake, and aldosterone actually fell below baseline levels when injections were terminated during sodium deprivation and while ACTH was administered during normal sodium intake.

From Newton and Laragh 675


Figure 24.

Renin system in normal subjects divided according to blood pressure and plasma renin levels. Analysis was carried out in 139 normal subjects divided into normotensive [n = 99, solid boxes and lines; diastolic blood pressure (DBP) < 85 mm Hg] and borderline hypertensive groups (n = 40, dashed boxes and lines; DBP 85–100 mm Hg). Each blood pressure group was subdivided on basis of renin level into low (<1 ng/ml/h, n = 14, 7), medium (1–5 ng/ml/h, n = 77, 26), or high (>5 ng/ml/h, n = 8, 7) renin groups. As expected, urine and plasma aldosterone followed renin levels. Nonetheless, differences in aldosterone between groups were not as great on a percentage basis; nor were they always statistically significant. Urine aldosterone to renin ratio (UA/PRA) was highest in both low renin groups and lowest in both high renin groups. This could not be ascribed to effect of potassium to stimulate aldosterone, because low renin groups did not have higher urine or serum potassium. Low renin subjects seem to have increased adrenal sensitivity to angiotensin II, but basis for this is unexplained.

From Sealey et al., unpublished data


Figure 25.

Illustration of link between sodium balance and blood pressure homeostasis and between sodium balance and potassium homeostasis. However, there is little evidence for link between potassium and blood pressure.



Figure 26.

Data from Figure 3 replotted to illustrate mean urinary sodium excretion for given ranges of plasma renin activity and urinary aldosterone excretion. Differences in sodium excretion are significant at all higher rates suggesting that angiotensin and aldosterone continue to exert regulatory effect on urinary sodium excretion even when circulating concentrations are low.

From Laragh et al. 544


Figure 27.

Periodic fluctuations in urine sodium excretion, sodium balance, plasma renin activity, and urine aldosterone excretion after initiation of high sodium diet (270 mEq), which was preceded by 11 days of sodium deprivation (10 mEq/day) (not shown here; see Fig. 30). Mean values ±SD from three normal subjects are presented. Each subject exhibited similar periodic fluctuation in urine sodium, renin, and aldosterone. After 4 days of diet, natriuresis occurred for 3 days, and these high levels of sodium excretion were associated with lowest levels of plasma renin activity and aldosterone excretion.

From Sealey et al. 827


Figure 28.

Demonstration that when angiotensin II is fixed during changes in sodium intake, blood pressure increases with sodium loading and is at its lowest level with sodium depletion. Changes in mean arterial pressure during chronic changes in sodium intake in control dogs and in dogs during angiotensin II blockade with the converting enzyme inhibitor SQ 14.225 or during angiotensin II infusion (5 mg‐kg−1.min) also shown. Values are means ±SE.

From Hall et al. 380


Figure 29.

Top: interrelationship of renin‐aldosterone hormonal system with changes in sodium and potassium balance. Bottom: coordination of intrarenal physical factors with hormonal factors for sodium and potassium homeostasis. Rate of excretion of each cation is determined by interaction of aldosterone with distal tubular sodium supply.

From Sealey and Laragh 838


Figure 30.

Effect of sodium depletion on urine aldosterone excretion and potassium balance–combined results from five normal subjects. Despite hyperaldosteronism induced by sodium depletion, potassium balance became progressively positive. Therefore, other factors (see Fig. 29) counterbalance kaliuretic action of aldosterone. Increase in aldosterone‐renin ratio most likely reflects gradual increase in potassium balance; this change was accompanied by only modest increases in plasma potassium.

From Laragh et al. 543


Figure 31.

Acute effects (at 90 min) of two different converting enzyme inhibitors, teprotide and captopril, on diastolic blood pressure. With both drugs, percent fall in blood pressure is closely related to pretreatment levels of plasma renin activity in quietly seated, untreated hypertensive patients. Note also that almost every subject exhibited some hypotensive response to drug, again illustrating (see Fig. 26) that even low levels of renin may have an effect. Left: effects of administering nonapeptide (isolated from snake venom) teprotide (SQ 20881), intravenously to 89 patients; data are replotted from Case et al. 173,175. Right: changes in seated diastolic blood pressure 90 min after single oral dose of 25 mg captopril to 166 patients; data are replotted from Case et al. 172 and Laragh et al. 532. Setting aside errors in cuff pressure measurements, data reveal remarkable and extremely similar correlations between height of pretreatment plasma renin value and degree of induced decrease in blood pressure. Note that patients with plasma renin values <1.0 ng/ml/h exhibited smallest change in pressure. Both sets of data also provide strong indirect evidence that plasma renin value reflects active role of renin in supporting arterial pressure in hypertensive persons.

Data replotted from Case et al. 172,173,175 and Laragh et al. 532


Figure 32.

Relationship between acute (60 min) fall in diastolic pressure and baseline renin in response to oral captopril (25–50 mg) in group of hypertensive patients divided into those with 30 min seated renins of <1, 1–6, or >6 ng/ml/h. The higher the baseline renin of each group, the greater the fall in diastolic pressure. On average, captopril lowered diastolic pressure by close to 20 mm Hg in the 74 high renin patients; fall was only 5 mm Hg in low renin group.

From Mueller et al. 647


Figure 33.

Serum levels of magnesium (left) and ionized calcium (right) in normotensive control subjects (N1 BP) and in different renin subgroups of essential hypertensive subjects. Low, medium, and high renin essential hypertension abbreviated as Lo RH, N1 RH, and Hi RH, respectively. For both cations, hypertensive patients differ significantly from normotensive controls. To convert to millimoles per liter, multiply by 0.5.

From Resnick et al. 776


Figure 34.

Relationship of the percent fall in systolic pressure during treatment with verapamil (120 mg, 3xday) to baseline ambulatory plasma renin activity in 13 hypertensive patients. Patients represented by circles were on low‐sodium intake (9 mEq/day); those represented by triangles were on a high‐sodium intake (212 mEq/day). Those on high‐sodium intake and those with lower plasma renin levels were more responsive to the calcium channel blocker.

From Nicholson et al. 681


Figure 35.

Cellular calcium hypothesis of hypertension that reconciles observed heterogeneous extracellular divalent cation levels among hypertensive patients with their presumed uniformly abnormal intracellular concentrations, ex, Extracellular calcium; cyt, cytosolic free calcium; BP, blood pressure.

From Resnick 772


Figure 36.

In two‐kidney, one‐clip renal hypertensive rats infusion of angiotensin receptor antagonist saralasin induced immediate fall in blood pressure, which reached −40.8±4.2 mm Hg after 60 min (P<0.001). In contrast, change in blood pressure induced in one‐kidney, one‐clip renal hypertensive rats was not significant (P>0.1).

From Brunner et al. 126


Figure 37.

In sodium‐depleted, one‐kidney, one‐clip renovascular hypertensive rats, infusion of angiotensin II antagonist saralasin produced striking falls in blood pressure. Twenty‐four hours later, after same animals were sodium repleted, there was no significant effect on blood pressure by same dose of antagonist. These studies illustrate dynamic relationship between sodium and renin in maintaining elevated blood pressure of this form of renovascular hypertension

From Gavras et al. 338


Figure 38.

Illustration that blood pressure reduction induced by angiotensin II blockade can be reversed by sodium loading in patient with malignant hypertension (studied under balance ward conditions). First vasoconstriction and then volume support to hypertension are shown. Angiotensin blockade with saralasin produced dramatic fall in blood pressure. However, as blockade was maintained, when sodium chloride was infused over next 40 h, blood pressure returned to high control values and excess volume replaced vasoconstriction in support of blood pressure. Administration of 40 mg Lasix (L40) during continued angiotensin II blockade resulted in diuresis and fall in blood pressure.

From Brunner et al. 125


Figure 39.

Metabolism balance study of patient with pseudoprimary aldosteronism. Dotted lines indicate intakes of potassium and sodium. Normal ranges for aldosterone secretion and for midday serum renin in ambient subjects for each dietary sodium intake are indicated by range bars. Aldosterone secretion was always markedly elevated, and serum renin levels were abnormally low. Responses of aldosterone and renin to manipulations in sodium intake were blunted. Potassium repletion was more easily accomplished when dietary sodium was reduced.

From Ledingham et al. 535


Figure 40.

Renal–adrenal axis is hormonal cascade involving renin, angiotensin, and aldosterone for regulation of sodium and potassium balance and blood pressure. Interaction is depicted as it was first discovered in studies of patients with malignant hypertension in whom, because of defective feedback, it is involved in causation. Accordingly, there is massive excess of both renin and aldosterone that cannot turn itself off.

From Laragh et al. 507


Figure 41.

Different high blood pressure mechanisms, pathophysiological changes, and treatment strategies in high and low renin hypertensive patients.

Adapted from Laragh et al. 512


Figure 42.

Different blood pressure mechanisms in two animal models of renovascular (i.e., Goldblatt) hypertension. Although comparable blood pressure elevation occurs in Goldblatt hypertension of either the one‐kidney or two‐kidney type, different mechanisms are involved. Volume overexpansion from impaired renal excretory capacity is implicated in one‐kidney type, whereas renin‐initiated vasoconstriction appears largely responsible for two‐kidney type.

From Laragh et al. 545


Figure 43.

Dramatic difference in 60‐min plasma renin response to single oral dose of converting enzyme inhibitor captopril between patients with essential hypertension and those with renovascular disease. Response is used as basis of screening test for renovascular hypertension.

From Mueller et al. 647


Figure 44.

Renal angioplasty reduces plasma renin activity into normal range in patients with renovascular hypertension. Left: before angioplasty; right: 6 months after angioplasty. Hatched area shows normal range of plasma renin in relation to concurrent 24 h urine sodium excretion.

From Pickering et al. 748


Figure 45.

Renal vein renin diagnostic patterns. In essential hypertension (top), renin level in each renal vein is ∼25% greater than peripheral arterial, venous, or infrarenal inferior vena caval renin at all levels of renin secretion. In setting of unilateral renin secretion (curable renovascular hypertension; bottom left), affected kidney is solely responsible for maintaining peripheral renin levels. Hence, increment is at least 50% (0.5) and becomes progressively greater as renal blood flow is reduced. Patients with unilateral secretion of renin and normal BUN and'serum creatinine can usually be cured by angioplasty, surgical repair, or nephrectomy. But, if BUN and serum creatinine are elevated, bilateral disease is likely, even if contralateral suppression of renin secretion is observed. Unequal bilateral renin secretion (bottom right) indicates bilateral disease and decreases change of cure following unilateral nephrectomy, but improvement or even cure may be possible following angioplasty or corrective surgery. V1, renal vein renin; V2, renal vein renin on opposite side; IVC, inferior vena caval renin. Bold face large numbers indicate levels of plasma renin at the sites indicated.

From Laragh & Seale 541


Figure 46.

Relation of noon ambulatory plasma renin activity (left) and corresponding daily urinary aldosterone excretion (right) to concurrent daily rate of urinary sodium excretion. Dashed lines outline normal channel derived from study of normotensive people (see Fig. 3). Total of 219 patients with untreated essential hypertension were studied, some on several occasions and at different levels of sodium intake. Three major subgroups (▴, low renin, ○, normal renin, and ▪, high renin essential hypertension) are defined by appropriateness or normalcy of plasma renin activity to rate of sodium excretion, used as index of dietary intake. Additional abnormal subgroups are defined when aldosterone (right) is included in the analysis.

From Brunner et al. 127


Figure 47.

Response to intravenous converting enzyme inhibition (MK 422) based on specific mechanisms of vasoconstriction. Left: High renin heart failure patient has prompt hemodynamic improvement following small dose of intravenous enalaprilat with further improvement in repeat challenge. Right: Low renin patient with comparable heart failure did not respond to intravenous enalaprilat but had prompt response to oral calcium channel inhibitor nifedipine (10 mg). Findings are representative of relative selectivity of response based on the mechanism of vasoconstriction. MAP, mean arterial pressure; PCWP, pulmonary capillary wedge pressure; CI, cardiac index; SVR, systemic vascular resistance.

From Cody et al. 196
References
 1. Abboud, H. E., R.‐G. Luke, J. H. Galla, and T. A. Kotchen. Stimulation of renin by acute selective chloride depletion in the rat. Circ. Res. 44: 815‐821, 1979.
 2. Abrams, J. S. Blood pressure response to the portal infusion of angiotensin II. Surg. Forum 17: 133‐134, 1966.
 3. Acker, G. M., F. X. Galen, C. Devaux, S. Foote, E. Papernik, A. Pesty, J. Menard, and P. Corvol. Human chorionic cells in primary culture: a model for renin biosynthesis. J. Clin. Endocrinol. Metab. 55: 902‐909, 1982.
 4. Addis, T., E. Barrett, R. I. Boyd, and H. J. Ureen. Renin proteinuria in the rat. I. The relation between the proteinuria and the pressor effect of renin. J. Exp. Med. 89: 131‐140, 1949.
 5. Addison, T. Disease of suprarenal capsules. Lond. Med. Gazette 43: 517, 1849.
 6. Africa, B., and E. Haber. The production and characterization of specific antibodies to aldosterone. Immunochemistry 8: 479‐486, 1961.
 7. Aguilera, G., and K. J. Catt. Regulation of aldosterone secretion by the renin‐angiotensin system during sodium restriction in rats. Proc. Natl. Acad. Sci. USA 75: 4057‐4061, 1978.
 8. Aguilera, G., and K. J. Catt. Loci of action of regulators of aldosterone biosynthesis in isolated glomerulosa cells. Endocrinology 104: 1046‐1052, 1979.
 9. Aguilera, G., K. Fujita, and K. J. Catt. Mechanisms of inhibition of aldosterone secretion by adrenocorticotropin. Endocrinology 108: 522‐528, 1981.
 10. Ajzen, H., U. Andrade, J. P. Cipullo, D. R. Sustovich, and D. L. Ramos. Effect of angiotensin II on urinary sodium excretion in normal subjects and in cirrhotic patients. Am. J. Med. Sci. 256: 373‐379, 1968.
 11. Akinkugbe, O. O., W. C. B. Brown, and W. I. Cranston. The direct renal action of angiotensin in the rabbit. Clin. Sci. 30: 259‐266, 1966.
 12. Akinkugbe, O. O., W. C. B. Brown, and W. I. Cranston. Response to angiotensin infusion before and after adrenalectomy in the rabbit. Am. J. Physiol. 212: 1147‐1152, 1967.
 13. Alderman, M. H., S. Madhavan, W. L. Ooi, H. Cohen, J. E. Sealey, and J. H. Laragh. High renin/sodium phenotype predicts myocardial infarction (MI): renin hypothesis confirmed, abstracted. Circulation 80 (Suppl. II): 101, 1989.
 14. Alexander, E. A., and N. G. Levinsky. An extrarenal mechanism of potassium adaptation. J. Clin. Invest. 47: 740‐748, 1968.
 15. Alexander, R. W., T. A. Brock, M. A. Gimbrone, Jr., and S. E. Rittenhouse. Angiotensin increases inositol trisphosphate and calcium in vascular smooth muscle. Hypertension 7: 447‐451, 1985.
 16. Ames, R. P., A. J. Borkowski, A. M. Sicinski, and J. H. Laragh. Prolonged infusions of angiotensin II and norepinephrine and blood pressure, electrolyte balance, aldosterone and cortisol secretion in normal man and in cirrhosis with ascites. J. Clin. Invest. 44: 1171‐1186, 1965.
 17. Anand‐Srivastava, M. B. Angiotensin II receptors negatively coupled to adenylate cyclase in rat aorta. Biochem. Biophys. Res. Commun. 117: 420‐428, 1983.
 18. Anderson, H. M., and J. H. Laragh. Renal excretion of potassium in normal and sodium depleted dogs. J. Clin. Invest. 37: 323‐331, 1958.
 19. Arakawa, K., M. Makatani, A. Minohora, and M. Nakamura. The isolation of human angiotensin. Circ. Res. 20/21 (Suppl. II): 101‐107, 1967.
 20. Assaykeen, T. A., P. L. Clayton, A. Goldfien, and W. G. Ganong. The effect of alpha‐ and beta‐adrenergic blocking agents on the renin response to hypoglycemia and epinephrine in dogs. Endocrinology 87: 1318‐1322, 1970.
 21. Assaykeen, T. A., K. Otsuka, and W. F. Ganong. Rate of disappearance of exogenous dog renin from the plasma of nephrectomized dogs. Proc. Soc. Exp. Biol. Med. 127: 306‐310, 1968.
 22. Atarashi, K., P. J. Mulrow, R. Franco‐Saenz, R. Snajdar, and J. Rapp. Inhibition of aldosterone production by an atrial extract. Science 224: 992‐994, 1984.
 23. Atlas, S. A., P. Christofalo, T. Hesson, J. E. Sealey, and L. C. Fritz. Immunological evidence that inactive renin is prorenin. Biochem. Biophys. Res. Commun. 132: 1038‐1045, 1985.
 24. Atlas, S. A., T. E. Hesson, J. E. Sealey, B. Dharmgrongartama, J. H. Laragh, M. C. Ruddy, and M. Aurell. Characterization of inactive renin (“prorenin”) from renin‐secreting tumors of nonrenal origin: similarity to inactive renin from kidney and normal plasma. J. Clin. Invest. 73: 437‐447, 1984.
 25. Atlas, S. A., and J. H. Laragh. Physiological actions of atrial natriuretic factor. In: Atrial Hormones and Other Natriuretic Factors, edited by P. J. Mulrow and R. Schrier. Bethesda: American Physiological Society, 1987, p. 53‐76.
 26. Atlas, S. A., R. L. Letcher, D. B. Case, T. G. Pickering, L. R. Resnick, E. D. Vaughan, Jr., J. E. Sealey, and J. H. Laragh. Aldosterone response to upright posture and converting enzyme inhibition in primary aldosteronism, abstracted. Clin. Res. 29: 565A, 1981.
 27. Atlas, S. A., J. E. Sealey, and T. E. Hesson. An inactive, prorenin‐like substance in human kidney and plasma. Clin. Sci. 59: 29s‐33s, 1980.
 28. Atlas, S. A., J. E. Sealey, T. E. Hesson, A. P. Kaplan, J. Menard, P. Corvol, and J. H. Laragh. Biochemical similarity of partially purified inactive renins from human plasma and kidney. Hypertension 4: 86s‐95s, 1982.
 29. Atlas, S. A., J. E. Sealey, T. E. Hesson, and J. H. Laragh. Apparent molecular size difference between plasma and renal inactive renins. Clin. Exp. Hypertens. [A] 4: 2039‐2047. 1982.
 30. Atlas, S. A., J. E. Sealey, J. H. Laragh, and C. Moon. Plasma renin and “prorenin” in essential hypertension during sodium depletion, beta‐blockade, and reduced arterial pressure. Lancet 2: 785‐789, 1977.
 31. Ayers, C. R. Plasma renin activity and renin‐substrate concentration in patients with liver disease. Circ. Res. 20: 594‐598, 1967.
 32. Ayers, C. R., J. O. Davis, F. Lieberman, C. C. J. Carpenter, and M. Berman. The effects of chronic hepatic venous congestion on the metabolism of d,l‐aldosterone and d‐aldosterone. J. Clin. Invest. 41: 884‐895, 1962.
 33. Ayers, C. R., R. H. Harris, Jr., and L. G. Lefer. Control of renin release in experimental hypertension. Circ. Res. 24/25 (Suppl. 1): 103‐112, 1969.
 34. Baer, L., F. J. Goodwin, and J. H. Laragh. Diazoxideinduced renin release in man: dissociation from plasma and extracellular fluid volume changes. J. Clin. Endocrinol. 29: 1107‐1109, 1969.
 35. Baer, L., S. C. Sommers, L. R. Krakoff, M. A. Newton, and J. H. Laragh. Pseudo‐primary aldosteronism: an entity distinct from true primary aldosteronism. Circ. Res. 26/27 (Suppl. 1): 203‐216, 1970.
 36. Bailey, J. R., and D. J. Randall. Renal perfusion pressure and renin secretion in the rainbow trout, Salmo gairdneri. Can. J. Zool. 59: 1220‐1226, 1981.
 37. Bakhle, Y. S. Conversion of angiotensin I to angiotensin II by cell‐free extracts of dog lung. Nature 220: 919‐920, 1968.
 38. Bakhle, Y. S., and J. R. Vane. Pharmacokinetic function of the pulmonary circulation. Physiol. Rev. 54: 1007‐1045, 1974.
 39. Balla, I., P. Enyedi, A. Spat, and F. A. Antoni. Pressor‐type vasopressin receptors in the adrenal cortex: properties of binding, effects on phosphoinositide metabolism and aldosterone secretion. Endocrinology 117: 421‐423, 1985.
 40. Bank, N., and H. S. Aynedjian. A micropuncture study of the renal concentrating defect of potassium depletion. Am. J. Physiol. 206: 1347‐1352, 1964.
 41. Barajas, L. Architecture of the juxtaglomerular apparatus. In: Hypertension: Pathophysiology, Diagnosis and Management, edited by J. H. Laragh and B. M. Brenner. New York: Raven, 1990, p. 1053‐1068.
 42. Barajas, L., and K. Powers. The structure of the juxtaglomerular apparatus (JGA) and the control of renin secretion: an update. J. Hypertens. 2 (Suppl. 1): 3‐12, 1984.
 43. Barajas, L., K. Powers, O. Carretero, A. G. Scicli, and T. Inagami. Immunocytochemical localization of renin and kallikrein in the rat renal cortex. Kidney Int. 29: 965‐970, 1986.
 44. Barbour, B. H., J. R. Gill, and F. C. Bartter. Effects of angiotensin on the toad skin. Proc. Soc. Exp. Biol. Med. 116: 806‐808, 1964.
 45. Barnardo, D. E., C. G. Strong, and W. P. Baldus. Failure of the cirrhotic liver to inactivate renin: evidence for a splanchnic source of renin‐like activity. J. Lab. Clin. Med. 74: 495‐506, 1969.
 46. Barraclough, M. A., N. F. Jones, and C. D. Marsden. Effect of angiotensin on renal function in the rat. Am. J. Physiol. 212: 1153‐1157, 1967.
 47. Barrett, J. D., P. Eggena, and M. P. Sambhi. Activation of rat plasma renin. Endocrinology 108: 778‐785, 1980.
 48. Bartter, F. C, A. G. T. Caspe, C. S. Delea, and J. D. H. Slater. On the role of the kidney in control of adrenal steroid production. Metab. Clin. Exp. 10: 1006‐1020, 1961.
 49. Bartter, F. C., I. H. Mills, E. G. Biglieri, and C. Delea. Studies on the control and physiological action of aldosterone. In: Recent Progress in Hormone Research, edited by G. Pincus. New York: Academic, 1959, vol. XV, p. 311‐344.
 50. Bartter, F. C., P. Pronove, J. R. Gill, and R. C. Mac‐Cardle. Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. Am. J. Med. 33: 811‐828, 1962.
 51. Baumann, E. J., and S. Kurland. Change in the inorganic constituents of the blood in suprarenalectomized cats and rabbits. J. Biol. Chem. 71: 281‐302, 1927.
 52. Beierwaltes, W. H., J. Prada, and O. A. Carretero. Effect of glandular kallikrein on renin release in isolated rat glomeruli. Hypertension 7: 27‐31, 1985.
 53. Beierwaltes, W. H., J. Prada, and O. A. Carretero. Kinin stimulation of renin release in isolated rat glomeruli. Am. J. Physiol. 248 (Renal Fluid Electrolyte Physiol. 17): F757‐F761, 1985.
 54. Bell, G. M., M. Pecker, S. A. Atlas, G. D. James, J. E. Sealey, and J. H. Laragh. Diurnal and postural variations in plasma ANF1 cGMP and sodium excretion, abstracted. Am J Hypertens. 1: 108A, 1988.
 55. Benelli, G., D. Della Bella, and A. Gandini. Angiotensin and peripheral sympathetic nerve activity. Br. J. Pharmacol. 22: 211‐219, 1964.
 56. Berg, T. J., J. Sulner, C. Y. Lai, and R. L. Soffer. Immunohistochemical localization of two angiotensin I‐converting isoenzymes in the reproductive tract of the male rabbit. J. Histochem. Cytochem. 34: 753‐760, 1986.
 57. Berliner, R. W., and C. M. Bennett. Concentration of urine in the mammalian kidney. Am. J. Med. 42: 777‐789, 1967.
 58. Berliner, R. W., T. J. Kennedy, Jr., and J. G. Hilton. Renal mechanisms for excretion of potassium. Am. J. Physiol. 162: 348‐367, 1950.
 59. Bianchi, A., A. F. de Schaepdryver, G. R. de Vleeschhouwer, and P. Preziosi. On the pharmacology of synthetic hypertensine. Arch. Int. Pharmacodyn. Ther. 124: 21‐44, 1960.
 60. Bickerton, R. K., and J. P. Buckley. Evidence for a central mechanism in angiotensin induced hypertension. Proc. Soc. Exp. Biol. Med. 106: 834‐841, 1961.
 61. Biglieri, E. G., M. Schambelan, and P. E. Slaton. Effect of adrenocorticotropin on desoxycorticosterone, corticosterone and aldosterone excretion. J. Clin. Endocrinol. Metab. 29: 1090‐1101, 1969.
 62. Bing, J. Mechanism of the increased sensitivity to renin in nephrectomized animals. Acta Pathol. Microbiol. Scand. 66: 311‐322, 1964.
 63. Bing, J., and K. Poulsen. Cause of increased plasma angiotensinogen after nephrectomy. Acta Pathol. Microbiol. Scand. 78 (Sect. A): 669‐673, 1970.
 64. Binnion, P. F., and J. D. Hatcher. Cardiovascular effects of infusions of epinephrine and angiotensin singly and in combination. Circ. Res. 12: 393‐398, 1963.
 65. Biron, P. Angiotensin infusions in an adrenalectomized patient. Rev. Can. Biol. 23: 473‐475, 1964.
 66. Biron, P., W. P. Baldus, and W. H. J. Summerskill. Plasma angiotensinase activity in cirrhosis. Proc. Soc. Exp. Biol. Med 116: 1074‐1077, 1964.
 67. Biron, P., M. Chretien, E. Koiw, and J. Genest. Effects of angiotensin infusions on aldosterone and electrolyte excretion in normal subjects and patients with hypertension and adrenocortical disorders. Br. Med. J. 1: 1569‐1575, 1962.
 68. Biron, P., and C. G. Huggins. Pulmonary activation of synthetic angiotensin I. Life Sci. 7: 965‐970, 1968.
 69. Biron, P., E. Koiw, W. Nowaczynski, J. Brouillet, and J. Genest. The effects of intravenous infusion of valine‐5‐angiotensin II and other pressor agents on urinary electrolyte and corticosteroids, including aldosterone. J. Clin. Invest. 40: 338‐347, 1961.
 70. Biron, P., R. Landesman, and J. C. Hunt. Plasma angiotensinase activity in human hypertension. Nature 204: 1096‐1112, 1964.
 71. Biron, P., P. Meyer, and J. C. Panisset. Removal of angiotensins from the systemic circulation. Can. J. Physiol. Pharmacol. 46: 175‐178, 1968.
 72. Bisset, G. E., and G. P. Lewis. A spectrum of pharmacological activity in some biologically active peptides. Br. J. Pharmacol. 19: 168‐182, 1962.
 73. Black, D. A. K., R. Platt, and S. W. Stanbury. Regulation of sodium excretion in normal and salt‐depleted subjects. Clin. Sci. 9: 205‐222, 1950.
 74. Blaine, E. H., and J. O. Davis. Evidence for a renal intravascular receptor for renin secretion. Am. J. Physiol. 220: 1593‐1597, 1971.
 75. Blaine, E. H., J. O. Davis, and J. S. Baumber. Plasma renin substrate changes in experimental uremia. Proc. Soc. Exp. Biol. Med. 136: 21‐24, 1971.
 76. Blaine, E. H., J. O. Davis, and R. T. Witty. Renin release after hemorrhage and after suprarenal aortic constriction in dogs without sodium delivery to the macula densa. Circ. Res. 27: 1081‐1089, 1970.
 77. Blair‐West, J. R., J. P. Coghlan, D. A. Denton, A. P. Gibson, C. J. Oddie, W. H. Sawyer, and B. A. Scoggins. Plasma renin activity and blood corticosteroids in the Australian lungfish, Neoceratodus forsteri. J. Endocrinol. 74: 137‐142, 1977.
 78. Blair‐West, J. R., J. P. Coghlan, D. A. Denton, J. R. Goding, J. A. Munro, R. E. Peterson, and M. Wintour. Humoral stimulation of adrenal cortical secretion. J. Clin. Invest. 41: 1606‐1627, 1962.
 79. Blank, S., J. E. West, F. B. Mueller, R. J. Cody, G. A. Harshfield, M. S. Pecker, J. H. Laragh, and T. G. Pickering. Wideband external pulse recording during cuff deflation: a new technique for evaluation of the arterial pressure pulse and measurement of blood pressure. Circulation 77: 1297‐1305, 1988.
 80. Blaufox, M. D., E. J. Lewis, P. Jagger, D. Lauler, R. Hickler, and J. P. Merrill. Physiologic responses of the transplanted human kidney. N. Engl. J. Med. 280: 62‐66, 1969.
 81. Bledsoe, T., G. W. Liddle, A. Riondel, D. P. Island, D. Bloomfield, and B. Sinclair‐Smith. Comparative fates of intravenously and orally administered aldosterone: evidence for extrahepatic formation of acid‐labile conjugate in man. J. Clin. Invest. 45: 264‐269, 1966.
 82. Bock, K. D., H. Dengler, H. J. Krecke, and G. Reichel. Untersuchungen uber die wirkung von synthetischem hypertensin II auf elektrolythaushalt, Nierenfunktion und Kreislauf beim menschen. Klin. Wochenschr. 36: 808‐814, 1958.
 83. Bock, K. D., and H. J. Krecke. Die wirkung von synthetischem hypertensin II auf die PAH und Insulin‐clearance die renale haemodynamik und die diurese beim Menschen. Klin. Wochenschr. 36: 69‐74, 1958.
 84. Bock, K. D., H. J. Krecke, and H. M. Kuhn. Untersuchungen uber die wirkung von synthetischem hypertensin II auf blutdruck, atmung und extremitatendurchblutung des Menschen. Klin. Wochenschr. 36: 254‐261, 1958.
 85. Boger, J. Renin inhibition. In: Annual Reports in Medicinal Chemistry, edited by D. M. Bailey. Orlando: Harcourt Brace Jovanovich, 1985, vol. 20, p. 257‐266.
 86. Bogin, E., S. G. Massry, and I. Harary. Effect of parathyroid hormone on rat heart cells. J. Clin. Invest. 67: 1215‐1227, 1981.
 87. Bojesen, E. Concentrations of aldosterone and corticosterone in peripheral plasma of rats: the effects of salt depletion, salt repletion, potassium loading and intravenous injections of renin and angiotensin II. Eur. J. Steroids 1: 145‐169, 1966.
 88. Bolli, P., F. W. Amann, and F. R. Buhler. Antihypertensive response to post‐synaptic alpha‐blockade with prazosin in low and normal renin. Hypertension 2: S399‐S405, 1980.
 89. Bolton, T. B. Mechanisms of action of transmitters and other substances on smooth muscle. Physiol. Rev. 59: 606‐718, 1979.
 90. Bonjour, J.‐P. and R. L. Malvin. Effect of angiotensin in the denervated kidney of the dog. Proc. Soc. Exp. Biol. Med. 131: 469‐473, 1969.
 91. Bonting, S. J., M. R. Canady, and N. M. Hawkins. Angiotensin and renal Na‐K activated adenosine triphosphatase: studies on Na‐K activated ATPase. VII. Biochim. Biophys. Acta 82: 427‐429, 1964.
 92. Borkowski, A. J., S. S. Howards, and J. H. Laragh. Angiotensin and electrolyte excretion in renovascular hypertension. Am. J. Physiol. 208: 1087‐1092, 1965.
 93. Bougas, J., C. Flood, B. Little, J. F. Tait, S. A. S. Tait, and R. Underwood. Dynamic aspects of aldosterone metabolism. In: Aldosterone, edited by E. E. Baulieu and P. Robel. Oxford: Blackwell, 1964, p. 25‐50.
 94. Bouhnik, J., J. A. Fehrentz, F. X. Galen, R. Seyer, G. Evin, B. Castro, J. Menard, and P. Corvol. Immunological identification of both plasma and human renal inactive renin as prorenin. J. Clin. Endocrinol. Metab. 60: 399‐401, 1985.
 95. Boyd, J. E., and P. J. Mulrow. Intracellular potassium: the regulator of aldosterone production, abstracted. J. Clin. Invest. 51: 13A, 1972.
 96. Boyd, J. E., W. P. Palmore, and P. J. Mulrow. Role of potassium in the control of aldosterone secretion in the rat. Endocrinology 88: 556‐565, 1971.
 97. Bradley, S. E. Physiology of essential hypertension. Am. J. Med. 4: 398‐415, 1948.
 98. Bradley, S. E., J. J. Curry, and G. P. Bradley. Renal extraction of p‐aminohippurate in normal subjects and essential hypertension and chronic diffuse glomerulonephritis. Federation Proc. 6: 79‐80, 1947.
 99. Brandis, M., J. Keyes, and E. E. Windhager. Potassium‐induced inhibition of proximal tubular fluid reabsorption in rats. Am. J. Physiol. 222: 421‐427, 1972.
 100. Brar, H. S., Y. S. Do, H. B. Tam, G. J. Valenzuela, R. D. Murray, L. D. Longo, M. L. Yonekura, and W. A. Hsueh. Uteroplacental unit as a source of elevated circulating prorenin levels in normal pregnancy. Am. J. Obstet. Gynecol. 155: 1223‐1226, 1986.
 101. Braun‐Menendez, E., J. C. Fasciolo, L. F. Leloir, and J. M. Munoz. La substancia hipertensora de la sangre del rinon isquemiado. Rev. Soc. Arg. Biol. 15: 420‐430, 1939.
 102. Braun‐Menendez, E., J. C. Fasciolo, L. F. Leloir, and J. M. Munoz. The substance causing renal hypertension. J. Physiol. 98: 283‐298, 1940.
 103. Braun‐Menendez, E., J. C. Fasciolo, L. F. Leloir, J. M. Munoz, and A. C. Taquini. Renal Hypertension. Springfield, IL: Thomas, 1946.
 104. Brenner, B. M., K. H. Falchuk, R. I. Keimowitz, and R. W. Berliner. The relationship between peritubular capillary protein and fluid reabsorption by the renal proximal tubule. J. Clin. Invest. 48: 1519‐1531, 1969.
 105. Brentjens, J. R., S. Matsuo, G. A. Andres, P. R. B. Caldwell, and L. Zamboni. Gametes contain angiotensin converting enzyme (kininase II). Experientia 42: 399‐402, 1986.
 106. Briggs, J. P., and J. Schnermann. Macula densa control of renin secretion and glomerular vascular tone: evidence for common cellular mechanisms. Renal. Physiol. 9: 193‐203, 1986.
 107. Brod, J., V. Fencl, Z. Hejl, J. Jirka, and M. Ulrych. General and regional haemodynamic pattern underlying essential hypertension. Clin. Sci. 23: 339‐349, 1962.
 108. Brodehl, J., and K. Dellissen. Die antidiuretische Wirkung des Angiotensins beim Diabetes insipidus. Klin. Wochenschr. 44: 101‐103, 1966.
 109. Brown, G. P., and J. G. Douglas. Angiotensin II binding sites on isolated rat renal brush border membranes. Endocrinology 111: 1830‐1836, 1982.
 110. Brown, G. P., and J. G. Douglas. Angiotensin II binding sites in rat and primate isolated renal tubular basolateral membranes. Endocrinology 112: 2007‐2014, 1983.
 111. Brown, J. A., J. A. Oliver, I. W. Henderson, and B. A. Jackson. Angiotensin and single nephron glomerular function in the trout, Salmo gairdneri. Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R509‐R514, 1980.
 112. Brown, J. J., G. Chapuis, and J. I. S. Robertson. The effect of long‐continued intravenous infusions of angiotensin in the rabbit. Lancet 1: 1356‐1357, 1963.
 113. Brown, J. J., G. Chapuis, and J. I. S. Robertson. The effect of prolonged intravenous infusion of angiotensin in the rabbit. Clin. Sci. 26: 165‐175, 1964.
 114. Brown, J. J., D. L. Davies, A. F. Lever, D. McPherson, and J. I. S. Robertson. Plasma renin concentration in relation to changes in posture. Clin. Sci. 30: 278‐284, 1966.
 115. Brown, J. J., D. L. Davies, A. F. Lever, and J. I. S. Robertson. Influence of sodium deprivation and loading on the plasma renin in man. J. Physiol. 173: 408‐419, 1964.
 116. Brown, J. J., D. L. Davies, A. F. Lever, and J. I. S. Robertson. Variation of plasma renin during a 24‐hour period. J. Endocrinol. 34: 129‐130, 1966.
 117. Brown, J. J., D. L. Davies, A. F. Lever, J. I. S. Robertson, and M. Tree. Estimation of renin in human plasma. Biochem. J. 93: 594‐600, 1964.
 118. Brown, J. J., D. L. Davies, A. F. Lever, J. I. S. Robertson, and A. Verniory. The effect of acute hemorrhage in the dog and man on plasma renin concentration. J. Physiol. 182: 649‐663, 1966.
 119. Brown, J. J., G. K. Matthew, and J. I. S. Robertson. The effects of angiotensin on the function of the separate kidneys in patients with unilateral renal artery stenosis. Clin. Sci. 26: 381‐395, 1964.
 120. Brown, J. J., and W. S. Peart. The effect of angiotensin on urine flow and electrolyte excretion in hypertensive patients. Clin. Sci. 22: 1‐17, 1962.
 121. Brown, S. R., G. A. Stephens, and M. J. Todt. Systemic and renal effects of angiotensin II in the freshwater turtle, Pseudemys scripta elegans. Am. J. Physiol. 245 (Regulatory Integrative Comp. Physiol. 14): R837‐R842, 1983.
 122. Brunner, D. B., G. Desponds, J. Biollaz, I. Keller, F. Ferber, H. Gavras, H. R. Brunner, and J. L. Schelling. Effect of a new angiotensin converting enzyme inhibitor MK 421 and its lysine analogue on the components of the renin system in healthy subjects. Br. J. Clin. Pharmacol. 11: 461‐467, 1981.
 123. Brunner, H. R., L. Baer, J. E. Sealey, J. G. Ledingham, and J. H. Laragh. The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects. J. Clin. Invest. 49: 2128‐2138, 1970.
 124. Brunner, H. R., H. Gavras, and J. H. Laragh. Angiotensin‐II blockade in man by sar1‐ala8‐angiotensin II for understanding and treatment of high blood‐pressure. Lancet 2: 1045‐1048, 1973.
 125. Brunner, H. R., H. Gavras, J. H. Laragh, and R. Keenan. Hypertension in man: exposure of the renin and sodium components using angiotensin II blockade. Circ. Res. 34 (Suppl. I): 35‐46, 1974.
 126. Brunner, H. R., J. D. Kirshman, J. E. Sealey, and J. H. Laragh. Hypertension of renal origin: evidence for two different mechanisms. Science 174: 1344‐1346, 1971.
 127. Brunner, H. R., J. H. Laragh, L. Baer, M. A. Newton, F. T. Goodwin, L. R. Krakoff, R. H. Bard, and F. R. Buhler. Essential hypertension: renin and aldosterone, heart attack and stroke. N. Engl. J. Med. 286: 441‐449, 1972.
 128. Brunner, H. R., J. E. Sealey, and J. H. Laragh. Renin subgroups in essential hypertension: further analysis of their pathophysiological and epidemiological characteristics. Circ. Res. 32 (Suppl. I): 99‐105, 1973.
 129. Brunner, H. R., J. E. Sealey, and J. H. Laragh. Renin as a risk factor in essential hypertension: more evidence. Am. J. Med. 55: 295‐302, 1973.
 130. Buhler, F. R. Antihypertensive actions of beta blockers. In: Frontiers in Hypertension Research, edited by J. H. Laragh, F.R. Buhler, and D. W. Seldin, . New York: Springer‐Verlag, 1981, p. 423‐435.
 131. Buhler, F. R. Calcium antagonists as first‐choice therapy for low‐renin essential hypertension. Kidney Int. 36: 295‐305, 1989.
 132. Buhler, F. R., U. L. Hulthen, W. Kiowski, and P. Bolli. The place of the calcium antagonist verapamil in antihypertensive therapy. J. Cardiovasc. Pharmacol. 4 (Suppl.): S350‐S357, 1982.
 133. Buhler, F. R., J. H. Laragh, L. Baer, E. D. Vaughan, Jr., and H. R. Brunner. Propranolol inhibition of renin secretion: a specific approach to diagnosis and treatment of renin‐dependent hypertensive diseases. N. Engl. J. Med. 287: 1209‐1214, 1972.
 134. Buhler, F. R., J. H. Laragh, J. E. Sealey, and H. R. Brunner. Plasma aldosterone‐renin interrelationships in various forms of essential hypertension: studies using a rapid assay of plasma aldosterone. Am. J. Cardiol. 32: 554‐561, 1973.
 135. Buhler, F. R., J. H. Laragh, E. D. Vaughan, Jr., H. R. Brunner, H. Gavras, and L. Baer. Antihypertensive action of propranolol. Specific antirenin responses in high and normal renin forms of essential, renal, renovascular and malignant hypertension. Am. J. Cardiol. 32: 511‐522, 1973.
 136. Buhler, F. R., J. E. Sealey, and J. H. Laragh. Radioimmunoassay of plasma aldosterone. In: Hypertension Manual, edited by J. H. Laragh. New York: Dun‐Donnelley, 1974, p. 655‐669.
 137. Bull, M. B., R. S. Hillman, P. J. Cannon, and J. H. Laragh. Renin and aldosterone secretion in man as influenced by changes in electrolyte balance and blood volume. Circ. Res. 27: 953‐960, 1970.
 138. Bumpus, F. M., H. Schwarz, and I. H. Page. Synthesis and pharmacology of the octapeptide angiotonin. Science 125: 886‐887, 1957.
 139. Bunag, R. B., I. H. Page, and J. W. McCubbin. Neural stimulation of release of renin. Circ. Res. 19: 851‐860, 1966.
 140. Burgess, E. D., P. M. Keane, and M. Watanabe. Blood pressure and serum calcium response to altered sodium intake in high renin hypertension. Am. J. Hypertens. 2: 182‐184, 1989.
 141. Burnstock, G., M. E. Holman, and C. L. Prosser. Electro‐physiology of smooth muscle. Physiol. Rev. 43: 482‐527, 1963.
 142. Byrom, F. B. The nature of malignancy in hypertensive disease: evidence from the retina of the rat. Lancet 1: 516‐520, 1963.
 143. Byrom, F. B. The Hypertensive Vascular Crisis: An Experimental Study. London: William Heinemann, 1969.
 144. Cade, J. R., and T. Perenich. Aldosterone production by rats, abstracted. Clin. Res. 12: 47, 1964.
 145. Caldwell, P. R. B., B. C. Seegal, K. C. Hsu, M. Das, and R. L. Soffer. Angiotensin‐converting enzyme: vascular endothelial localization. Science 191: 1050‐1051, 1976.
 146. Camargo, M. J. F., S. A. Atlas, and T. Maack. Role of increased glomerular filtration rate in atrial natriuretic disease in hypertensive patients. Life. Sci. 38: 2397‐2404, 1986.
 147. Camargo, M. J. F., H. D. Kleinert, S. A. Atlas, J. E. Sealey, J. H. Laragh, and T. Maack. Calcium‐dependent hemodynamic and natriuretic effects of atrial extract in isolated rat kidney. Am. J. Physiol. 246 (Renal Fluid Electrolyte Physiol. 15): F447‐F456, 1984.
 148. Camargo, M. J. F., N. V. Lutterotti, M. S. Pecker, G. D. James, P. B. M. W. M. Timmermans, and J. H. Laragh. Dup 753 increases survival in spontaneously hypertensive stroke‐prone rats fed a high sodium diet. Am. J. Hypertens. 4: 341S‐345S, 1991.
 149. Camargo, M. J. F., M. Volpe, M. S. Pecker, J. E. Sealey, and J. H. Laragh. Sodium induced increase and potassium induced fall in both plasma renin activity and stroke in stroke prone spontaneously hypertensive rats, abstracted. Kidney Int. 35: 324a, 1989.
 150. Camilleri, J‐P., V. N. Phat, J. Bariety, P. Corvol, and J. Menard. Use of a specific antiserum for renin detection in human kidney. J. Histochem. Cytochem. 28: 1343‐1346, 1980.
 151. Campbell, W. B., M. G. Currie, and P. Needleman. Inhibition of aldosterone biosynthesis by atriopeptins in rat adrenal cells. Circ. Res. 57: 113‐118, 1985.
 152. Cannon, P. J., R. P. Ames, and J. H. Laragh. Indirect action of angiotensin infusion to inhibit renal tubular sodium reabsorption in dogs. Am. J. Physiol. 211: 1021‐1030, 1966.
 153. Cannon, P. J., R. P. Ames, and J. H. Laragh. Relation between potassium balance and aldosterone secretion in normal subjects and in patients with hypertensive or renal tubular disease. J. Clin. Invest. 45: 865‐879, 1966.
 154. Cannon, P. J., J. M. Leeming, S. C. Sommers, R. W. Winters, and J. H. Laragh. Juxtaglomerular cell hyperplasia and secondary hyperaldosteronism (Bartter's syndrome): a re‐evaluation of the pathophysiology. Medicine (Baltimore) 47: 107‐131, 1968.
 155. Cannon, P. J., W. B. Stason, F. E. Demartini, S. C. Sommers, and J. H. Laragh. Hyperuricemia in primary and renal hypertension. N. Engl. J. Med. 275: 457‐464, 1966.
 156. Capelli, J. P., L. G. Wesson, G. E. Aponte, C. Faraldo, and E. Jaffe. Characterization and source of a renin‐like enzyme in anephric human. J. Clin. Endocrinol. Metab. 28: 221‐230, 1968.
 157. Capponi, A., U. Lang, M. Rossier, A. Riondel, and M. B. Vallotton. Intracellular mediators of aldosterone production: the role of cytosolic free calcium and protein kinase C. In: Corticosteroids and Peptide Hormones in Hypertension, edited by F. Mantero and P. Vecsei. New York: Raven, 1987, p. 59‐66.
 158. Carey, R. M., and S. Sen. Recent progress in the control of aldosterone secretion. Recent Prog. Horm. Res. 42: 251‐289, 1986.
 159. Carmines, P. K., T. K. Morrison, and L. G. Navar. Angiotensin II effects on microvascular diameters of in vitro blood‐perfused juxtamedullary nephrons. Am. J. Physiol. 251: 610‐618, 1986.
 160. Carmines, P. K., and L. G. Navar. Disparate effects of Ca channel blockade on afferent and efferent arteriolar responses to ANG II. Am. J. Physiol. 256 (Renal Fluid Electrolyte Physiol. 25): F1015‐F1029, 1989.
 161. Carmines, P. K., M. D. Perry, J. B. Hazelrig, and L. G. Navar. Effects of preglomerular and postglomerular vascular resistance alterations on filtration fraction. Kidney Int. 31 (Suppl. 20): S229‐S232, 1987.
 162. Carpenter, C. C. J., J. O. Davis, and C. R. Ayers. Relation of renin, angiotensin II and experimental renal hypertension to aldosterone secretion. J. Clin. Invest. 40: 2026‐2042, 1961.
 163. Carpenter, C. C. J., J. O. Davis, and C. R. Ayers. Concerning the role of arterial baroreceptors in the control of aldosterone secretion. J. Clin. Invest. 40: 1160‐1171, 1961.
 164. Carr, A. A., and L. M. Prisant. The calcium antagonist, isradipine, and its effect on blood pressure related to plasma renin activity. Am. J. Hypertens. 3: 354‐359, 1990.
 165. Carretero, O., and F. Gross. Renin substrate in plasma under various experimental conditions in the rat. Am. J. Physiol. 213: 695‐700, 1967.
 166. Carretero, O. A., and W. H. Beierwaltes. Effect of glandular kallikrein, kinins and aprotinin (a serine protease inhibitor) on renin release. J. Hypertens. 2 (Suppl. 1): 125‐130, 1984.
 167. Carrick, S., and R. J. Balment. The renin‐angiotensin system and drinking in the euryhaline flounder, Platichthys flesus. Gen. Comp. Endocrinol. 51: 423‐433, 1983.
 168. Carroll, R. G., T. E. Lohmeier, and A. J. Brown. Chronic angiotensin II infusion decreases renal norepinephrine overflow in conscious dogs. Hypertension 6: 675‐681, 1984.
 169. Carroll, R. G., and D. F. Opdyke. Evolution of angiotensin II‐induced catecholamine release. Am. J. Physiol. 243 (Regulatory Integrative Comp. Physiol. 12): R65‐R69, 1982.
 170. Casals‐Stenzel, J., M. Tree, J. J. Brown, R. Fraser, A. F. Lever, J. A. Millar, J. J. Morton, J. I. S. Robertson, J. L. Reid, and C. Hamilton. Prolonged infusion of norepinephrine in the conscious dog: effects on blood pressure, heart rate, angiotensin II, and aldosterone. J. Cardiovasc. Pharmacol. 4: S114‐S121, 1982.
 171. Casals‐Stenzel, J., M. Tree, J. J. Brown, R. Fraser, A. F. Lever, J. A. Millar, J. J. Morton, J. I. S. Robertson, J. L. Reid, and C. Hamilton. Effects of prolonged and brief infusions of noradrenaline on arterial pressure and on the plasma concentrations of active renin, angiotensin II, aldosterone, and potassium. J Hypertens. 1: 27‐35, 1983.
 172. Case, D. B., S. A. Atlas, J. H. Laragh, J. E. Sealey, P. A. Sullivan, and D. N. McKinstry. Clinical experience with blockade of the renin‐angiotensin‐aldosterone system by an oral converting‐enzyme inhibitor (SQ 14,225, captropril) in hypertensive patients. Prog. Cardiovasc. Dis. 21: 195‐206, 1978.
 173. Case, D. B., J. M. Wallace, H. J. Keim, J. E. Sealey, and J. H. Laragh. Usefulness and limitations of saralasin, a partial competitive agonist of angiotensin, for evaluating the renin and sodium factors in hypertensive patients. Am. J. Med. 60: 825‐836, 1976.
 174. Case, D. B., J. M. Wallace, H. J. Keim, M. A. Weber, J. I. Drayer, R. P. White, J. E. Sealey, and J. H. Laragh. Estimating renin participation in hypertension: superiority of converting enzyme inhibitor over saralasin. Am. J. Med. 61: 790‐796, 1976.
 175. Case, D. B., J. M. Wallace, H. J. Keim, M. A. Weber, J. E. Sealey, and J. H. Laragh. Possible role of renin in hypertension as suggested by renin‐sodium profiling and inhibition of converting enzyme. N. Engl. J. Med. 296: 641‐646, 1977.
 176. Casellas, D., P. K. Carmines, and L. G. Navar. Microvascular reactivity of in vitro blood perfused juxtamedullary nephrons from rats. Kidney Int. 28: 752‐759, 1985.
 177. Catt, K. J. Molecular mechanisms of hormone action: control of target cell function by peptide, steroid, and thyroid hormones. In: Endocrinology and Metabolism, edited by P. Felig, J. D. Baxter, A. E. Broadus, and L. A. Frohman. New York: McGraw‐Hill, 1987, p. 82‐165.
 178. Catt, K. J., M. C. Cain, J. P. Coghlan, P. Z. Zimmet, E. Cran, and J. B. Best. Metabolism and blood levels of angiotensin II in normal subjects, renal disease, and essential hypertension. Circ. Res. 26: 177‐193, 1970.
 179. Chan, M. Y., and W. H. Holmes. Studies on a “renin‐angiotensin” system in the normal and hypophysectomized pigeon (Columba livia). Gen. Comp. Endocrinol. 16: 304‐311, 1971.
 180. Chartier, L., E. Schiffrin, G. Thibault, and R. Garcia. Atrial natriuretic factor inhibits stimulation of aldosterone secretion by angiotensin II, ACTH, and potassium in vitro and All‐induced steroidogenesis in vivo. Endocrinology 115: 2026‐2028, 1984.
 181. Chasis, H., W. Goldring, E. Breed, A. Bolomey, and H. W. Smith. Effects of salt and protein restriction on blood pressure and renal hemodynamics in hypertensive patients. J. Clin. Invest. 28: 775‐70, 1949.
 182. Chaudhari, A., B. Badio‐Dezfooly, B. M. Homadani, and L. G. Fine. Stimulation of Na‐H antiport by angiotensin II in the proximal tubular cell is mediated by PGE2. Abstract, The American Society of Nephrologists, 17th Meeting, 156A, 1984.
 183. Chesley, L. C., E. Talledo, C. S. Bohler, and F. Zuspan. Vascular reactivity to angiotensin II and norepinephrine in pregnant and nonpregnant women. Am. J. Obstet. Gynecol. 91: 837‐842, 1965.
 184. Cheville, R. A., J. A. Luetscher, E. W. Hancock, A. J. Dowdy, and G. W. Nokes. Distribution, conjugation and excretion of labeled aldosterone in congestive heart failure and in controls with normal circulation: development and testing of a model with an analog computer. J. Clin. Invest. 45: 1302‐1316, 1966.
 185. Chiu, A. T., J. V. Duncia, D. E. McCall, P. C. Wong, W. A. Price, M. J. M. C. Thoolen, D. J. Carini, A. L. Johnson, and P. B. M. W. M. Timmermans. Nonpeptide angiotensin II receptor antagonists. III. Structure‐function studies. J. Pharmacol. Exp. Ther. 250: 867‐874, 1989.
 186. Chiu, A. T., W. F. Herblin, D. E. McCall, R. J. Ardecky, D. J. Carini, J. V. Duncia, L. J. Pease, P. C. Wong, R. R. Wexler, A. L. Johnson, and P. B. M. W. M. Timmermans. Identification of angiotensin II receptor subtypes. Biochem. Biophys. Res. Commun. 165: 196‐203, 1989.
 187. Chiu, A. T., D. E. McCall, W. A. Price, P. C. Wong, D. J. Carini, J. V. Duncia, R. R. Wexler, S. E. Yoo, A. L. Johnson and P. B. M. W. M. Timmermans. Nonpeptide angiotensin II receptor antagonists. VII. Cellular and biochemical pharmacology of DuP 753, an orally active antihypertensive agent. J. Pharmacol. Exp. Ther. 252 (2): 711‐718, 1990.
 188. Chiu, P. J. S., and E. J. A. Sommer. Effect of Na+ restriction on blood pressure responses to beta‐adrenoreceptor blockade in spontaneously hypertensive rats (SHR), abstracted. Federation Proc. 38: 2372, 1979.
 189. Christy, N. P., and J. H. Laragh. Pathogenesis of hypokalemic alkalosis in Cushing's syndrome. N. Engl. J. Med. 265: 1083‐1088, 1961.
 190. Churchill, P. C. Ca‐dependence of the inhibitory effect of K‐depolarization on renin secretion from rat kidney slices. Arch. Int. Pharmacodyn. Ther. 258: 300‐312, 1982.
 191. Churchill, P. C. Second messengers in renin secretion. Am. J. Physiol. 249 (Renal Fluid Electrolyte Physiol. 18): F175‐F184, 1985.
 192. Churchill, P. C. A1 and A2 adenosine receptor activation inhibits and stimulates renin secretion of rat renal cortical slices. J. Pharmacol. Exp. Ther. 232: 589‐594, 1985.
 193. Ciccone, C. D., and E. J. Zambraski. Effects of phenoxybenzamine, metoprolol, captopril, and medofenamate on cardiovascular function in deoxycorticosterone acetate: hypertensive Yucatan miniature swine. Can. J. Physiol. Pharmacol. 61: 149‐153, 1985.
 194. Cody, R. J., S. A. Atlas, J. H. Laragh, S. H. Kubo, A. B. Covit, K. S. Ryman, A. Shaknovich, K. Pondolfino, M. Clark, M. J. Camargo, G. L. Schaer, and J. A. Lewicki. Atrial natriuretic factor in normal subjects and heart failure patients: plasma levels and renal, hormonal, and hemodynamic responses to peptide infusion. J. Clin. Invest. 78: 1362‐1374, 1986.
 195. Cody, R. J., A. B. Covit, G. L. Schaer, J. H. Laragh, J. E. Sealey, and J. Feldschuh. Sodium and water balance in chronic congestive heart failure. J. Clin. Invest. 77: 1441‐1452, 1986.
 196. Cody, R. J., J. H. Laragh, S. A. Atlas, and D. B. Case. Converting enzyme inhibition to identify and treat reninmediated or sodium‐volume related forms of increased peripheral resistance in hypertension and in congestive heart failure. J. Hypertens. 1 (Suppl. 1): 77‐84, 1983.
 197. Cohn, J. N. Relationship of plasma volume changes to resistance and capacitance vessel effects of sympathomimetic amines and angiotensin in man. Clin. Sci. 30: 267‐278, 1966.
 198. Coleman, T. G., and A. Guyton. Hypertension caused by salt loading in the dog. III. Onset transience of cardiac output and other circulatory occurrences. Circ. Res. 25: 153‐160, 1969.
 199. Collste, P., K. Haglund, G. Lundgren, G. Magnusson, and J. Ostman. Reversible renal failure during treatment with captopril. Br. Med. J. 2: 612‐613, 1979.
 200. Conn, J. W. Primary aldosteronism, a new clinical syndrome. J. Lab. Clin. Med. 45: 3‐17, 1955.
 201. Conn, J. W. Primary aldosteronism. J. Lab. Clin. Med. 45: 661‐664, 1955.
 202. Conn, J. W. Plasma renin activity in primary aldosteronism: importance in differential diagnosis and in research of essential hypertension. JAMA 190: 222‐225, 1964.
 203. Conn, J. W., R. F. Knopf, and R. M. Nesbit. Clinical characteristics of primary aldosteronism from an analysis of 145 cases. Am. J. Surg. 107: 159‐172, 1964.
 204. Conn, J. W., D. R. Rovner, E. L. Cohen, and R. M. Nesbit. Normokalemic primary aldosteronism: a detectable cause of curable hypertension. JAMA 193: 200‐206, 1965.
 205. Cook, W. F., and M. R. Lee. The preparation of rabbit renin substrate for the assay of minute amounts of renin. Biochem. J. 96: 413‐418, 1965.
 206. Coppage, W. S., D. P. Island, Jr., A. E. Cooner, and G. W. Liddle. The metabolism of aldosterone in normal subjects and in patients with hepatic cirrhosis. J. Clin. Invest. 41: 1672‐1680, 1962.
 207. Cortney, M., M. Mylle, W. E. Lassiter, and C. W. Gottschalk. Renal tubular transport of water, solute and PAH in rats loaded with isotonic saline. Am. J. Physiol. 209: 1199‐1205, 1965.
 208. Corvol, P., and J. Menard. Renin inhibition: immunological procedures and renin inhibitor peptides. Kidney Int. 34 (Suppl. 26): S73‐S79, 1988.
 209. Corvol, P., F. Pinet, F. X. Galen, P. F. Plouin, G. Chatellier, J. Y. Pagny, P. Bruneval, J. P. Camilleri, and J. Menard. Primary reninism. In: Hypertension: Pathophysiology, Diagnosis and Management, edited by J. H. Laragh and B. M. Brenner. New York: Raven, 1990, p. 1573‐1582.
 210. Coviello, A., and J. Crabbe. Effect of angiotensin II on active transport of sodium by toad bladder and skin. Biochem. Pharmacol. 14: 1739‐1744, 1965.
 211. Cowley, A. W., and J. W. Declue. Quantification of baroreceptor influence on arterial pressure changes seen in primary angiotensin‐induced hypertension in dogs. Circ. Res. 39: 779‐787, 1976.
 212. Cox, H. M., K. A. Munday, and J. A. Poat. Location of [125I]angiotensin II receptors on rat kidney cortex cells. Br. J. Pharmacol. 82: 891‐895, 1984.
 213. Crabbe, J. In: The Sodium Retaining Action of Aldosterone, edited by S. A. Arscia. Brussels: Presses Acad Europeene, 1963.
 214. Crane, J. K., C. P. Campanile, and J. C. Garrison. The hepatic angiotensin II receptor. J. Biol. Chem. 257: 4959‐4965, 1982.
 215. Craven, D. J., A. Y. Warren, and E. M. Symonds. Active and inactive renin in human seminal plasma. Arch. Androl. 7: 63‐67, 1981.
 216. Cushing, H. The basophil adenomas of the pituitary body and their clinical manifestations (pituitary basophilism). Bull. John Hopkins Hosp. 50: 137‐195, 1932.
 217. Cushman, D. W., and H. S. Cheung. Concentration of angiotensin‐converting enzyme in tissues of the rat. Biochim. Biophys. Acta 250: 261‐265, 1971.
 218. Cushman, D. W., F. L. Wang, W. C. Fung, C. M. Harvey, and J. M. Deforrest. Differentiation of angiotensin‐converting enzyme (ACE) inhibitors by their selective inhibition of ACE in physiologically important target organs. Am. J. Hypertens. 2: 294‐306, 1989.
 219. Cushman, P., Jr. Inhibition of aldosterone secretion by ouabain in dog adrenal tissue. Endocrinology 84: 808‐813, 1969.
 220. Cuthbert, M. F., A. W. Asscher, and J. H. Jones. Characterization of a vascular permeability factor or renal origin. Clin. Sci. 31: 325‐336, 1966.
 221. Dalakos, T. G., G. H. Anderson, and D. H. P. Streeten. Mechanism of the hypertension in Cushing's syndrome, abstracted. Clin. Res. 24: 271A, 1976.
 222. Dandridge, P.F., and S. F. Echtenkamp. Neural control of renin secretion in the primate, abstracted. FASEB J. 2: A986, 1988.
 223. Darby, I.A., P. Aldred, R. J. Crawford, R. T. Fernley, H. D. Niall, J. D. Penschow, G. B. Ryan, and J. P. Coghlan. Renin gene expression in vessels of the ovine renal cortex. J. Hypertens. 3: 9‐11, 1985.
 224. Das, M., and R. L. Soffer. Pulmonary angiotensin‐converting enzyme: structural and catalytic properties. J. Biol. Chem. 250: 6762‐6768, 1975.
 225. Daugharty, T. M., I. F. Ueki, D. P. Nicholas, and B. M. Brenner. Renal response to chronic intravenous salt loading in the rat. J. Clin. Invest. 52: 21‐31, 1973.
 226. Davies, R., R. Wiggins, J. D. H. Slater, and D. Geddes. Nature of the adrenoceptor that mediates renin release in man. Cardiovasc. Med. 3: 571‐575, 1978.
 227. Davignon, J., R. R. Lorenz, and J. T. Shepherd. Response of human umbilical artery to changes in transmural pressure, angiotensin and bradykinin. Am. J. Physiol. 209: 51‐59, 1965.
 228. Davis, J. O. Mechanisms of salt and water retention in congestive heart failure: the role of aldosterone. Am. J. Med. 29: 486‐507, 1960.
 229. Davis, J. O. Mechanisms regulating the secretion and metabolism of aldosterone in experimental secondary hyperaldosteronism. Recent Prog. Horm. Res. 17: 293‐352, 1961.
 230. Davis, J. O. Regulation of aldosterone secretion. In: Handbook of Physiology. Adrenal Gland, edited by H. Blaschko, G. Sayers, and A. D. Smith. Washington, DC: Am. Physiol. Soc. 1975, vol. V, p. 77‐106.
 231. Davis, J. O., C. R. Ayers, and C. C. J. Carpenter. Renal origin of an aldosterone stimulating hormone in dogs with thoracic caval constriction and in sodium‐depleted dogs. J. Clin. Invest. 40: 1466‐1474, 1961.
 232. Davis, J. O., C. C. J. Carpenter, C. R. Ayers, and R. C. Bahn. Relation of anterior pituitary function to aldosterone and corticosterone secretion in conscious dogs. Am. J. Physiol. 199: 212‐216, 1960.
 233. Davis, J. O., C. C. J. Carpenter, C. R. Ayers, and R. C. Bahn. Evidence for secretion of an aldosterone‐stimulating hormone by the kidney. J. Clin. Invest. 40: 684‐696, 1961.
 234. Davis, J. O., J. Urquhart, And J. T. Higgins, Jr. The effects of alterations of plasma sodium and potassium concentration on aldosterone secretion. J. Clin. Invest. 42: 597‐609, 1963.
 235. Day, M.D., J. W. Mc Cubbin, And I. H. Page. Limited hypertensive effect of infusion of angiotensin. Am. J. Physiol. 209: 264‐268, 1965.
 236. Day, R. P., And J. A. Luetscher. Big renin: a possible prohormone in kidney and plasma of a patient with Wilms' tumor. J. Clin. Endocrinol. Metab. 38: 923‐926, 1974.
 237. Deane, H. G., And G. M. C. Masson. Adrenal cortical changes in rats with various types of experimental hyptertension. J. Clin. Endocrinol. 11: 193‐208, 1951.
 238. DeBono, E., G. D. J. Lee, F. R. Mottram, G. W. Pickering, J. J. Brown, H. Keen, W. S. Peart, And P. H. Sanderson. The action of angiotensin in man. Clin. Sci. 25: 123‐157, 1963.
 239. DeChamplain, J., J. Genest, R. Veyrat, And R. Boucher. Factors controlling renin in man. Arch. Intern. Med. 117: 355‐363, 1966.
 240. DelGreco, F. Comparative effects of valine‐5 angiotensin II amide and pitressin on renal excretory function in diabetes insipidus. Proc. Soc. Exp. Biol. Med. 109: 105‐110, 1962.
 241. DelGreco, F., J. Roguska, And N. M. Simon. Angiotensin II infusion in renal disease with hypertension. Am. J. Med. Sci. 251: 323‐327, 1966.
 242. DeMartini, F. E. Hyperuricaemia induced by drugs. Arthritis Rheum. 8: 823‐829, 1965.
 243. Deming, Q. B., And J. A. Luetscher, Jr. Bioassay of desoxycorticosterone‐like material in urine. Proc. Soc. Exp. Biol. Med. 73: 171‐175, 1950.
 244. Dengler, H., And G. Reichel. Untersuchungen zur intrazellularen lokalisation der renin‐ und hypertensinase‐aktivitat. Experientia 16: 36‐38, 1960.
 245. Deodhar, S. D., F. E. Cuppage, And E. Gableman. Studies on the mechanism of experimental proteinuria induced by renin. J. Exp. Med. 120: 677‐690, 1964.
 246. Depasquale, N. P., And G. E. Burch. Angiotensin II, digital blood flow, and the precapillary and postcapillary blood vessels of man. Ann. Intern. Med. 58: 278‐292, 1963.
 247. Depasquale, N. P., And G. E. Burch. Effect of angiotensin II on the intact forearm veins of man. Circ. Res. 13: 239‐245, 1963.
 248. Derkx, F. H. M., A. T. Alberda, F. H. de Jong, F. H. Zeilmaker, J. W. Makovitz, And M. A. D. H. Schalekamp. Source of plasma prorenin in early and late pregnancy: observations in a patient with primary ovarian failure. J. Clin. Endocrinol. Metab. 65: 349‐354, 1987.
 249. Derkx, F. H. M., B. N. Bouma, M. P. A. Schalekamp, And M. A. D. H. Schalekamp. An intrinsic factor XII‐prekallikrein‐dependent pathway activates the human plasma renin‐angiotensin system. Nature 280: 315‐316, 1979.
 250. Derkx, F. H. M., J. M. G. Van Gool, G. J. Wenting, R. A. Verhoeven, A. J. Man In't Veld, And M. A. D. H. Schalekamp. Inactive renin in human plasma. Lancet 2: 496‐499, 1976.
 251. Derkx, F. H. M., G. J. Wenting, A. J. Man In't Veld, R. P. Verhoeven, And M. A. D. H. Schalekamp. Control of enzymatically inactive renin in man under various pathological conditions: implications for the interpretation of renin measurements in peripheral and renal venous plasma. Clin. Sci. Mol. Med. 54: 529‐538, 1978.
 252. Deschepper, C. F., And W. F. Ganong. Renin and angiotensin in endocrine glands. In: Frontiers in Neuroendocrinology, edited by L. Martini and W. F. Ganong. New York: Raven, 1988, vol. 10, p. 79‐98.
 253. Deschepper, C. F., S. H. Mellon, F. Cumin, J. D. Baxter, And W. F. Ganong. Analysis by immunocytochemistry and in situ hybridization of renin and its mRNA in kidney, testis, adrenal and pituitary of the rat. Proc. Natl. Acad. Sci. USA 83: 7552‐7556, 1986.
 254. Deth, R., And C. Van Breemen. Agonist induced release of intracellular Ca++ in the rabbit aorta. J. Membr. Biol. 30: 363‐380, 1977.
 255. Devaux, C., P. Meyer, J. M. Idatte, And P. Milliez. Influence of bilateral nephrectomy on the renin‐angiotensin system in man. Nephron 6: 612‐627, 1969.
 256. Dexter, L., H. A. Frank, F. W. Haynes, And M. D. Altschule. Traumatic shock. VI. The effect of haemorrhagic shock on the concentration of renin and hypertensinogen in the plasma in unanesthetized dogs. J. Clin. Invest. 22: 847‐852, 1943.
 257. Dickinson, C. J., And J. R. Lawrence. A slowly developing pressor response to small concentrations of angiotensin: its bearing on pathogenesis of chronic renal hypertension. Lancet 1: 1354‐1356, 1963.
 258. Dickinson, C. J., And R. Yu. Mechanisms involved in the progressive pressor response to very small amounts of angiotensin in conscious rabbits. Circ. Res. 21 (Suppl. II): 157‐163, 1967.
 259. Dickinson, C. J., And R. Yu. The progressive pressor response to angiotensin in the rabbit. J. Physiol. 190: 91‐99, 1967.
 260. Dirks, J. H., W. J. Cirksena, And R. W. Berliner. The effect of saline infusion on sodium reabsorption by the proximal tubule of the dog. J. Clin. Invest. 44: 1160‐1170, 1965.
 261. Doi, Y., K. Atarashi, R. Franco‐Saenz, And P. J. Mulrow. Effect of changes in sodium or potassium balance, and nephrectomy, on adrenal renin and aldosterone concentrations. Hypertension 6 (Suppl. I): 124‐129, 1984.
 262. Doolittle, R. F. Angiotensinogen is related to the antitrypsin‐antithrombin‐ovalbumin family. Science 222: 417‐419, 1983.
 263. Dorer, F. E., K. E. Lentz, J. R. Kahn, M. Levine, And L. T. Skeggs. A comparison of the substrate specificities of cathepsin D and pseudorenin. J. Biol. Chem. 253: 3140‐3142, 1978.
 264. Douglas, J., And K. J. Catt. Regulation of angiotensin II receptors in the rat adrenal cortex by dietary electrolytes. J. Clin. Invest. 58: 834‐843, 1976.
 265. Douglas, J., S. Saltman, P. Fredlund, T. Kondo, And K. J. Catt. Receptor binding of angiotensin II and antagonists: correlation with aldosterone production by isolated adrenal glomerulosa cells. Circ. Res. 38 (Suppl. II): 108‐112, 1976.
 266. Drayer, J. I., H. J. Keim, M. A. Weber, D. B. Case, And J. H. Laragh. Unexpected pressor responses to propranolol in essential hypertension: an interaction between renin, aldosterone and sympathetic activity. Am. J. Med. 60: 897‐903, 1976.
 267. Dresel, P., And I. Wallentin. Effects of sympathetic vasoconstrictor fibres, noradrenaline and vasopressin on the intestinal vascular resistance during constant blood flow or blood pressure. Acta Physiol. Scand. 66: 427‐436, 1966.
 268. Dudek, G., Z. S. Latallo, J. Prokopowicz, And K. Worowski. Degradation of angiotensin II by plasmin. Br. J. Pharmacol. 45: 60‐63, 1972.
 269. Dufau, M. L., and B. Kliman. Pharmacologic effects of angiotensin II‐amide on aldosterone and corticosterone secretion by the intact anesthetized rat. Endocrinology 82: 29‐36, 1968.
 270. Dunn, M. J. Renal prostaglandins: influence of sodium balance on the ability of diuretics to inhibit tubular reabsorption. In: Contemporary Issues in Nephrology, edited by B. M. Brenner and J. H. Stein. New York: Churchill Livingstone, 1979, vol. 4, p. 89‐114.
 271. Dzau, V. J., K. E. Ellison, T. Brody, J. Ingelfinger, and R. E. Pratt. A comparative study of the distributions of renin and angiotensinogen messenger ribonucleic acids in rat and mouse tissues. Endocrinology 120: 2334‐2338, 1987.
 272. Dzau, V. J., M. Mudgett‐Hunter, G. Kapler, and E. Haber. Monoclonal antibodies binding renal renin. Hypertension 3 (Suppl. II): 4‐8, 1981.
 273. Earley, L. E., and R. M. Friedler. The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium. J. Clin. Invest. 45: 542‐551, 1966.
 274. Earley, L. E., M. H. Humphreys, and E. Bartoli. Capillary circulation as a regulator of sodium reabsorption and excretion. Circ. Res. 31 (Suppl. 2): 1‐18, 1972.
 275. Edelman, I. S. Candidate mediators in the action of aldosterone on sodium transport. Membr. Transp. Proc. 1: 125‐140, 1978.
 276. Eilers, E. A., and R. E. Peterson. Aldosterone secretion in the rat. In: Aldosterone, edited by E. E. Baulieu and P. Robel. Philadelphia: Davis, 1964, p. 251‐264.
 277. Eisalo, A., M. Viranko, and P. I. Halonen. Effects of intravenous infusions of valine‐5‐angiotensin on urinary sodium and chlorides in aortic coarctation. Am. J. Cardiol. 11: 609‐612, 1963.
 278. El‐Dorry, H. A., H. G. Bull, K. Iwata, N. A. Thornberry, E. H. Cordes, and R. L. Soffer. Molecular and catalytic properties of rabbit testicular dipeptidyl carboxypeptidase. J. Biol. Chem. 257: 14128‐14133, 1982.
 279. El‐Dorry, H. A., C. B. Pickett, J. A. McGregor, and R. L. Soffer. Tissue‐specific expression of mRNAs for dipeptidyl carboxypeptidase isoenzymes. Proc. Natl. Acad. Sci. USA 79: 4295‐4297, 1982.
 280. Elkin, M., and C. Meng. The effects of angiotensin on renal vascularity in dogs. Am. J. Roentgenol. Radium Ther. Nucl. Med. 98: 927‐934, 1966.
 281. Elliot, D. F., and W. S. Peart. Amino acid sequence in a hypertensin. Nature 177: 527‐528, 1956.
 282. Elliot, D. F., and W. S. Peart. The amino acid sequence in a hypertensin. Biochem. J. 65: 246‐254, 1957.
 283. Emerson, T. E., Jr. Effects of angiotensin, epinephrine, norepinephrine and vasopressin on venous return. Am. J. Physiol. 210: 933‐942, 1966.
 284. Erdos, E. G., and R. A. Skidgel. The unusual substrate specificity and the distribution of human angiotensin I converting‐enzyme. Hypertension 8 (Suppl. I): 34‐37, 1986.
 285. Erlanger, B. F., F. Borek, S. M. Bieser, and S. Lieberman. Steroid protein conjugates. I. Preparation and characterization of conjugates of bovine serum albumin with testosterone and with cortisone. J. Biol. Chem. 228: 713‐727, 1957.
 286. Erne, P., P. Bolli, O. Bertel, U. L. Hulthen, W. Kiowski, F. B. Mueller, and F. R. Buhler. Factors influencing the hypertensive effects of calcium antagonists. Hypertension 5 (Suppl. II): 97‐102, 1983.
 287. Erne, P., P. Bolli, E. Burgisser, and F. R. Buhler. Correlation of platelet calcium with blood pressure: effect of antihypertensive therapy. N. Engl. J. Med. 310: 1084‐1088, 1984.
 288. Faber, J. E., and M. J. Brody. Central nervous system action of angiotensin during onset of renal hypertension in awake rats. Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H349‐H360, 1984.
 289. Fakunding, J. L., R. Chow, and K. J. Catt. The role of calcium in the stimulation of aldosterone production by adrenocorticotropin, angiotensin II, and potassium in isolated glomerular cells. Endocrinology. 105: 327‐333, 1979.
 290. Farrel, G. H. The physiological factors which influence the secretion of aldosterone. Recent Prog. Horm. Res. 15: 275‐297, 1959.
 291. Farrow, P. R., and R. Wilkinson. Reversible renal failure during treatment with captopril. Br. Med. J. 1: 1680, 1979.
 292. Fasola, A. F., B. L. Martz, and O. M. Helmer. Renal activity during supine exercise in normotensives and hypertensives. J. Appl. Physiol. 21: 1709‐1712, 1966.
 293. Feldberg, W., and G. P. Lewis. Further studies on the effects of peptides on the suprarenal medulla of cats. J. Physiol. 178: 239‐251, 1965.
 294. Fernandez, L. A., B. C. Tarlatzis, P. J. Rzasa, V. J. Caride, N. Laufer, A. F. Negro‐Vilar, A. H. Decherney, and F. Naftolin. Renin‐like activity in ovarian follicular fluid. Fertil. Steril. 44: 219‐223, 1985.
 295. Fernandez‐Repollet, E., E. Tapia, and M. Martinez‐Maldonado. Effects of angiotensin‐converting enzyme inhibition on altered renal hemodynamics induced by low protein diet in the rat. J. Clin. Invest. 80: 1045‐1049, 1987.
 296. Ferrebee, J. W., D. Parker, W. H. Carnes, M. K. Gerity, D. W. Atchley, and R. F. Loeb. Certain effects of desoxy‐corticosterone, development of “diabetes insipidus” and replacement of muscle potassium by sodium in normal dogs. Am. J. Physiol. 135: 230‐237, 1941.
 297. Ferrebee, J. W., C. Ragan, D. W. Atchley, and R. F. Loeb. Desoxycorticosterone esters: certain effects in treatment of Addison's disease. JAMA 133: 1725‐1731, 1939.
 298. Ferreira, S. H. Bradykinin potentiating factor (B.P.F.) present in venom of Bothrops jararaca. Br. J. Pharmacol. 24: 163‐169, 1965.
 299. Ferris, T. F., P. Gorden, and P. J. Mulrow. Rabbit uterus as a source of renin. Am. J. Physiol. 212: 698‐702, 1967.
 300. Ferris, T. F., and E. K. Weir. Effect of captopril on uterine blood flow and prostaglandin E synthesis in the pregnant rabbit. J. Clin. Invest. 71: 809‐815, 1983.
 301. Figueiredo, J. F., G. T. Conti, D. Falkenstein, D. Sigulem, and O. L. Ramos. Tetracaine, procaine and verapamil inhibition of fluid absorption in isolated perfused rabbit proximal convoluted tubules. Brz. J. Med. Biol. Res. 15: 259‐264, 1982.
 302. Finnerty, F. A., Jr. Hemodynamics of angiotensin in man. Circulation 25: 255‐258, 1962.
 303. Fishman, M. C., E. A. Zimmerman, and E. E. Slater. Renin and angiotensin: the complete system within the neuroblastoma X glioma cell. Science 214: 921‐923, 1981.
 304. Fitzsimons, J. T. Angiotensin stimulation of the central nervous system. Rev. Physiol. Biochem. Pharmacol. 87: 117‐167, 1980.
 305. Flood, C., D. Layne, M. S. Ramcharan, E. Rossipal, J. F. Tait, and S. A. S. Tait. An investigation of the urinary metabolites and secretion rates of aldosterone and cortisol in man and a description of methods for their measurement. Acta Endocrinol. 36: 237‐264, 1961.
 306. Folkow, B., B. Johansson, and S. Mellander. The comparative effects of angiotensin and noradrenaline on consecutive vascular sections. Acta Physiol. Scand. 53: 99‐104, 1961.
 307. Fontoura, B. M. A., D. R. Nussenzveig, P. B. M. W. M. Timmermans, and T. Maack. DuP 753 is a potent nonpeptide antagonist of angiotensin II receptors in isolated perfused rat kidney and cultured renal cells. Am. J. Hypertens. 4: 303S‐308S, 1990.
 308. Fordis, C. M., J. S. Megorden, R. G. Ropchak, and H. R. Keiser. Absence of renin‐like activity in rat aorta and micro‐vessels. Hypertension 5: 635‐641, 1983.
 309. Fowler, N. O., and J. C. Holmes. Coronary and myocardial actions of angiotensin. Circ. Res. 14: 191‐201, 1964.
 310. Foyle, L. V., Jr., and T. V. Feichtmeir. Adrenal cortical carcinoma producing solely mineralocorticoid effect. Am. J. Med. 19: 966‐975, 1955.
 311. Franklin, G. O., A. J. Dowd, B. V. Caldwell, and L. Speroff. The effect of angiotensin II intravenous infusion on plasma renin activity and prostaglandins A, E and F levels in the uterine vein of the pregnant monkey. Prostaglandins 6: 261‐280, 1974.
 312. Fray, J. C. S., and D. J. Lush. Stretch receptor hypothesis for renin secretion: the role of calcium. J. Hypertens. 2 (Suppl. 1): 19‐23, 1984.
 313. Fray, J. C. S., D. J. Lush, and A. N. D. Valentine. Cellular mechanisms of renin secretion. Federation Proc. 42: 3150‐3154, 1983.
 314. Freeman, R. H., J. O. Davis, and A. A. Seymour. Volume and vasoconstriction in experimental renovascular hypertension. Federation Proc. 41: 2409‐2414, 1982.
 315. Freeman, R. H., J. O. Davis, and D. Villarreal. Role of renal prostaglandins in the control of renin release. Circ. Res. 54: 1‐9, 1984.
 316. Friedland, J., C. Setton, and E. Silverstein. Angiotensin‐converting enzyme: induction by steroids in rabbit alveolar macrophages in culture. Science 197: 64‐65, 1977.
 317. Friedman, P. A., J. F. Figueiredo, T. Maack, and E. E. Windhager. Sodium–calcium interactions in the renal proximal convoluted tubule of the rabbit. Am. J. Physiol. 240 (Renal Fluid Electrolyte Physiol. 9): F558‐F568, 1981.
 318. Fritz, L. C., P. A. Ponte, A. E. Arfsten, D. F. Catanzaro, G. G. Rousseau, P. H. Eliard, S. Mellon, F. Cumino, J. Shine, J. D. Baxter, and T. L. Reudelhuber. Expression of the human renin gene, abstracted. Clin. Res. 34: 643A, 1986.
 319. Fujita, K., G. Aguilera, and K. J. Catt. The role of cyclic AMP in aldosterone production by isolated zona glomerulosa cells. J. Biol. Chem. 254: 8567‐8574, 1979.
 320. Funder, J. W., J. R. Blair‐West, J. P. Coghlan, D. A. Denton, B. A. Scoggins, and R. D. Wright. Effect of plasma (K+) on the secretion of aldosterone. Endocrinology 85: 381‐384, 1969.
 321. Furspan, P. B., G. J. Rinaldi, K. Hoffmann, and D. F. Bohr. Dietary calcium and cell membrane abnormality in genetic hypertension. Hypertension 13: 727‐730, 1989.
 322. Gafford, J. T., R. A. Skidgel, E. G. Erdos, and L. B. Hersh. Human kidney “enkephalinase,” a neutral metalloen‐dopeptidase that cleaves active peptides. Biochemistry 22: 3265‐3271, 1983.
 323. Galen, F. X., C. Devaux, S. A. Atlas, T. Guyenne, J. Menard, P. Corvol, D. Simon, C. Cazaubon, P. Richer, G. Badouaille, J. P. Richaud, P. Gros, and B. Pau. New monoclonal antibodies directed against human renin: powerful tools for the investigation of the renin system. J. Clin. Invest. 74: 723‐735, 1984.
 324. Galen, F. X., C. Devaux, A. M. Houot, J. Menard, P. Corvol, M. T. Corvol, M. C. Gubler, F. Mounier, and J. P. Camilleri. Renin biosynthesis by human tumoral juxtaglomerular cells. Evidences for a renin precursor. J. Clin. Invest. 73: 1144‐1155, 1984.
 325. Galen, F. X., T. T. Guyenne, C. Devaux, C. Auzan, P. Corvol, and J. Menard. Direct radioimmunoassay of human renin. J. Clin. Endocrinol. Metab. 48: 1041‐1043, 1979.
 326. Gallagher, J. F., J. H. Laragh, S. A. Atlas, and J. E. Sealey. Effect of trypsin or acid treatment on dog plasma renin activity measurements. Endocrinology. 107: 147‐154, 1980.
 327. Galli‐Gallardo, S. M., and R. Gallardo. Action of angiotensin and autonomic innervation in amphibian kidney, abstracted. In: Int. Symp. on Comp. Endocrinol., 9th, Hong Kong. 1981, p. 172.
 328. Ganguly, A., G. A. Melada, J. A. Luetscher, and A. J. Dowdy. Control of plasma aldosterone in primary aldosteronism: distinction between adenoma and hyperplasia. J. Clin. Endocrinol. Metab. 37: 765‐775, 1973.
 329. Gantt, C. L., and W. J. Carter. Acute effects of angiotensin on calcium, phosphorus, magnesium and potassium excretion. Can. Med. Assoc. J. 90: 287‐291, 1964.
 330. Gardes, J., J. Bouhnik, E. Clauser, P. Corvol, and J. Menard. Role of angiotensinogen in blood pressure homeostasis. Hyptertension 4: 185‐189, 1982.
 331. Garg, L. C., M. A. Knepper, and M. B. Burg. Mineralocorticoid effects on Na‐K‐ATPase in individual nephron segments. Am. J. Physiol. 240 (Renal Fluid Electrolyte Physiol. 9): F536‐F544, 1981.
 332. Garg, L. C., and N. L. Narang. Effects of aldosterone on NEH‐sensitive ATPase in rabbit nephron segments. Kidney Int. 34: 13‐17, 1988.
 333. Garthoff, B., and P. Bellemann. Effects of salt loading and nitrendipine treatment on dihydropryidine receptors in hypertensive rats, abstracted. The International Society on Hypertension, 11th Meeting, 1986.
 334. Garty, H. Mechanisms of aldosterone action in tight epithelia. J. Membr. Biol. 90: 193‐205, 1986.
 335. Garvin, J. L. Inhibition of Jv by ANF in rat proximal straight tubules requires angiotensin. Am. J. Physiol. 257 (Renal Fluid Electrolyte Physiol. 26): F907‐F911, 1989.
 336. Gaudino, N.M. Los suprarrenales en la hipertension arterial nefrogena. Ref. Soc. Arg. Biol. 20: 470‐486, 1944.
 337. Gavras, H., H. R. Brunner, J. H. Laragh, J. E. Sealey, I. Gavras, and R. A. Vukovich. An angiotensin converting‐enzyme inhibitor to identify and treat vasoconstrictor and volume factors in hypertensive patients. N. Engl. J. Med. 291: 817‐821, 1974.
 338. Gavras, H., H. R. Brunner, E. D. Vaughan, Jr., and J. H. Laragh. Angiotensin‐sodium interaction in blood pressure maintenance of renal hypertensive and normotensive rats. Science 180: 1369‐1371, 1973.
 339. Geller, R. G., and J. E. Kendrick. Flow responses to angiotensin in innervated and denervated kidneys. Proc. Soc. Exp. Biol. Med. 129: 727‐730, 1968.
 340. Genest, J., P. Biron, E. Korw, W. Nowaczynski, M. Chretien, and R. Boucher. Adrenocortical hormones in human hypertension and their relation to angiotensin. Circ. Res. 9: 775‐791, 1961.
 341. Genest, J., E. Korw, W. Nowaczynski, and T. Sandor. Study of urinary adrenocortical hormones in human hypertension and their relation to angiotensin, abstracted. Int. Congr. Endocrinol. Copenhagen, 1960, p. 173.
 342. Giebisch, G., E. L. Boulpaep, and G. Whittenbury. Electrolyte transport in kidney tubule cells. Philos. Trans. R. Soc. Lond. [Biol.] 262: 175‐196, 1971.
 343. Gill, J. R., Jr. Bartter's syndrome. In: Renal Tubular Disorders, edited by H. C. Gonick and V. M. Buckalew, Jr. New York: Dekker, 1985, p. 457‐468.
 344. Glenner, G. G., P. J. McMillan, and L. F. Folk. A mammalian peptidase specific for the hydrolysis of N‐terminal and L‐glutamyl and aspartic residues. Nature 194: 867‐872, 1962.
 345. Glorioso, N., S. A. Atlas, J. H. Laragh, R. Jewelewicz, and J. E. Sealey. Prorenin in high concentrations in human ovarian follicular fluid. Science 233: 1422‐1424, 1986.
 346. Glorioso, N., P. Madeddu, P. Dessi‐Fulgheri, A. Fois, F. Meloni, F. Bandiera, G. C. Tonolo, and A. Rappelli. Trypsin activatable renin in rat plasma. Clin. Sci. 64: 137‐140, 1983.
 347. Glorioso, N., C. Troffa, J. H. Laragh, S. A. Atlas, D. Marion, and J. E. Sealey. The cat: an animal model for studies of inactive renin. Am. J. Physiol. 252 (Endocrinol. Metab. 21): E509‐E518, 1987.
 348. Gocke, D. J., J. N. Gerten, L. M. Sherwood, and J. H. Laragh. Physiological and pathological variations of plasma angiotensin II in man: correlation with renin activity and sodium balance. Circ. Res. 24 (Suppl. I): 131‐148, 1969.
 349. Goldblatt, H. Studies on experimental hypertension: production of the malignant phase of hypertension. J. Exp. Med. 67: 809‐826, 1938.
 350. Goldblatt, H., Y. J. Katz, H. A. Lewis, and E. Richardson. Studies on experimental hypertension: production of persistent elevation of systolic blood pressure by means of renal ischemia. J. Exp. Med. 59: 347‐379, 1934.
 351. Goldblatt, H., Y. J. Katz, H. A. Lewis, and E. Richardson. Studies on experimental hypertension. XX. The bioassay of renin. J. Exp. Med. 77: 309‐314, 1943.
 352. Goldenberg, M., K. L. Pines, E. D. Baldwin, D. G. Greene, and C. E. Roh. The hemodynamic response of man to norepinephrine and epinephrine and its relation to the problem of hypertension. Am. J. Med. 5: 792‐806, 1948.
 353. Goldring, W., H. Chasis, H. A. Ranges, and H. W. Smith. Effective renal blood flow in subjects with essential hypertension. J. Clin. Invest. 20: 637‐653, 1941.
 354. Goodfriend, T. L., M. Elliott, and S. A. Atlas. Actions of synthetic atrial natriuretic factor on bovine adrenal glomerulosa. Life Sci. 35: 1675‐1682, 1984.
 355. Goodwin, F. J., J. D. Kirshman, J. E. Sealey, and J. H. Laragh. Influence of the pituitary gland on sodium conservation, plasma renin and renin substrate concentrations in the rat. Endocrinology 86: 824‐834, 1970.
 356. Goodwin, F. J., J. G. Ledingham, and J. H. Laragh. The effects of prolonged administration of vasopressin and oxytocin on renin, aldosterone and sodium balance in normal man. Clin. Sci. 39: 641‐651, 1970.
 357. Goormaghtigh, N. Les segments neuro‐myoarteriels juxta‐glomerularies du rein. Arch. Biol. (Leige) 43: 575‐591, 1932.
 358. Goormaghtigh, N. La Fonction Endocrine des Arterioles Renales. Louvian: Librarie Fonteyn, 1944.
 359. Goormaghtigh, N., and K. S. Grimson. Vascular changes in renal ischemia, cell mitosis in the media of arteries. Proc. Soc. Exp. Biol. Med. 42: 227‐228, 1939.
 360. Gordon, D. B., and I. N. Sachin. Chromatographic separation of multiple renin substrates in women: effect of pregnancy and oral contraceptives. Proc. Natl. Acad. Sci. USA 156: 461‐464, 1977.
 361. Gordon, R. D., L. K. Wolfe, D. P. Island, and G. W. Liddle. A diurnal rhythm in plasma renin activity in man. J. Clin. Invest. 45: 1587‐1592, 1965.
 362. Gould, A. B., L. T. Skeggs, and J. R. Kahn. The presence of renin activity in blood vessel walls. J. Exp. Med. 119: 389‐399, 1964.
 363. Gould, A. B., L. T. Skeggs, and J. R. Kahn. Measurement of renin and substrate concentrations in human serum. Lab. Invest. 15: 1802‐1813, 1966.
 364. Greene, J. A., A. J. Vander, and R. S. Kowalczyk. Plasma renin activity and aldosterone excretion after hemotransplantation. J. Lab. Clin. Med. 71: 586‐595, 1968.
 365. Greenlee, W. J. Renin inhibitors. Pharmaceut. Res. 4: 364‐374, 1987.
 366. Gross, F. Renin and hypertensin, physiologische oder pathologische Wirkstoffe? Klin. Wochenschr. 36: 693‐706, 1958.
 367. Gross, F., J. Lazar, and H. Orth. Inhibition of the renin‐angiotensinogen reaction by pepstatin. Science 175: 656, 1972.
 368. Gross, F., and H. Turrian. Pharmacology of hypertensin and synthetic analogues. In: Polypeptides Which Affect Smooth Muscles and Blood Vessels, edited by M. Schachter. Oxford: Pergamon, 1960, p. 137‐151.
 369. Gross, M. D., R. J. Grekin, T. C. Gniadek, and J. Z. Villareal. Suppression of aldosterone by cyproheptadine in idiopathic aldosteronism. N. Engl. J. Med. 305: 181‐185, 1981.
 370. Haas, E., and H. Goldblatt. Indirect assay of plasma renin. Lancet 1: 1330‐1332, 1972.
 371. Haber, E., T. Koerner, L. B. Page, B. Kliman, and A. Purnode. Application of a radioimmunoassay for angiotensin I to the physiologic measurements of plasma renin activity in normal human subjects. J. Clin. Endocrinol. Metab. 29: 1349‐1355, 1969.
 372. Haber, E., L. B. Page, and G. A. Jacoby. Synthesis of antigenic branch‐chain copolymers of angiotensin and poly‐L‐lysine. Biochemistry 4: 693‐698, 1965.
 373. Hackenthal, E., K. Aktories, and K. H. Jakobs. Pertussis toxin attenuates angiotensin II—induced vasoconstriction and inhibition of renin release. Mol. Cell. Endocrinol. 42: 113‐117, 1985.
 374. Hall, C. E., and S. Hungerford. Prevention of DOCA‐salt hypertension with the calcium blocker nitrendipine. Clin. Exp. Hypertens. A5: 721‐728, 1983.
 375. Hall, J. E. Regulation of glomerular filtration rate and sodium excretion by angiotensin II. Federation Proc. 45: 1431‐1437, 1986.
 376. Hall, J. E. Control of sodium excretion by angiotensin II: intrarenal mechanisms and blood pressure regulation. Am. J. Physiol. 250 (Regulatory Integrative Comp. Physiol. 19): R960‐R972, 1986.
 377. Hall, J. E., and J. P. Granger. Role of peripheral sympathetic nervous system in mediating chronic blood pressure and renal hemodynamic effects of angiotensin II, abstracted. Federation Proc. 42: 589, 1983.
 378. Hall, J. E., and A. C. Guyton. Changes in renal hemodynamics and renin release caused by increased plasma oncotic pressure. Am. J. Physiol. 231: 1550‐1556, 1976.
 379. Hall, J. E., A. C. Guyton, M. J. Smith, Jr., and T. G. Coleman. Chronic blockade of angiotensin II formation during sodium deprivation. Am. J. Physiol. 237 (Renal Fluid Electrolyte Physiol. F424‐F432, 1979.
 380. Hall, J. E., A. C. Guyton, M. J. Smith, Jr. and T. G. Coleman. Blood pressure and renal function during chronic changes in sodium intake: role of angiotensin. Am. J. Physiol. 239 (Renal Fluid Electrolyte Physiol. 8): F271‐280, 1980.
 381. Hall, L. E., and S. Hungerford. Prevention of DOCA‐salt hypertension with the calcium blocker nitrendipine. Clin. Exp. Hypertens. [A] 5: 721‐728, 1983.
 382. Halliday, M. A., and T. J. Egan. Changes in GFR and CH2O before and after repair of potassium deficiency. Am. J. Physiol. 202: 773‐776, 1962.
 383. Hallin, L., L. Andren, and L. Hansson. Controlled trial of nifedipine and budroflumenthiazide in hypertension. J. Cardiovasc. Pharmacol. 5: 1083‐1085, 1983.
 384. Haning, R., S. A. S. Tait, and J. F. Tait. In vitro effects of ACTH, angiotensins, serotonin and potassium on steroid output and conversion of corticosterone to aldosterone by isolated adrenal cells. Endocrinology 87: 1147‐1167, 1970.
 385. Hannon, R. C., R. P. Deruyck, J. V. Joossens, and A. K. Amery. Disappearance rate of endogenous renin from the plasma after bilateral nephrectomy in humans. J. Clin. Endocrinol. 29: 1420‐1424, 1969.
 386. Hardman, J. A., Y. J. Hort, D. F. Catanzaro, J. T. Tellam, J. D. Baxter, B. J. Morris, and J. Shine. Primary structure of the human renin gene. DNA 3: 457‐468, 1984.
 387. Harris, P. J., and L. G. Navar. Tubular transport responses to angiotensin: editorial review. Am. J. Physiol. 248 (Renal Fluid Electrolyte Phisiol. 17): F621‐F630, 1985.
 388. Harris, P. J., D. Thomas, and T. O. Morgan. Atrial natriuretic peptide inhibits angiotensin‐stimulated proximal tubular sodium and water reabsorption. Nature 326: 697‐698, 1987.
 389. Harris, P. J., and J. A. Young. Dose‐dependent stimulation and inhibition of proximal tubular sodium reabsorption by angiotensin II in the rat kidney. Pflugers Arch. 367: 295‐297, 1977.
 390. Harris, R. B., and I. B. Wilson. Sequencing of an active‐site peptide of angiotensin I‐converting enzyme containing an essential glutamic acid residue. J. Biol. Chem. 260: 2208‐2211, 1985.
 391. Harrop, G. A., A. Weinstein, L. J. Soffer, and J. H. Trescher. The diagnosis and treatment of Addison's disease. JAMA 100: 1850‐1855, 1933.
 392. Haynes, F. W., and L. Dexter. Renal humoral pressor mechanism in man. IV. The hypertensinogen content of plasma of normal patients and patients with various diseases. J. Clin. Invest. 24: 78‐81, 1945.
 393. Haynes, F. W., and L. Dexter. Renin hypertensinogen, and hypertensinase concentrations of blood of dogs during the development of hypertension by constriction of the renal artery. Am. J. Physiol. 150: 190‐196, 1947.
 394. Haynes, F. W., P. H. Forsham, and D. M. Hume. Effects of ACTH, cortisone, desoxycorticosterone and epinephrine on the plasma hypertensinogen and renin concentration of dogs. Am. J. Physiol. 172: 265‐275, 1953.
 395. Hayslett, J. P., M. Kashgarian, and F. Epstein. Changes in proximal and distal tubular reabsorption produced by rapid expansion of extracellular fluid. J. Clin. Invest. 46: 1254‐1263, 1967.
 396. Hazon, N., and I. W. Henderson. Factors affecting the secretory dynamics of 1‐alpha‐hydroxycorticosterone in the dogfish, Scyliorhinus canicula. Gen. Comp. Endocrinol. 59: 50‐55, 1985.
 397. Heacox, R., A. M. Harvey, and A. J. Vander. Hepatic inactivation of renin. Circ. Res. 21: 149‐152, 1967.
 398. Healy, J. K., C. Barcena, and G. E. Schreiner. Effect of angiotensin on maximal tubular transport of PAH and glucose in dogs. Am. J. Physiol. 209: 651‐654, 1965.
 399. Healy, J. K., J. B. Suszkiw, and V. W. Dennis. Effect of aldosterone and salt intake on renal and pressor actions of angiotensin. Nephron 3: 329‐343, 1966.
 400. Heidenreich, O., and Y. Kook. Die Beeinflussung des Kohlenhydrat‐ und Fettstoffwechsels durch Dauerin‐fusionen von Oxytocin, Vasopressin und Hypertensin. Arch. Exp. Pathol. Pharmacol. 245: 280‐281, 1963.
 401. Helmer, O. M., and R. S. Griffith. Biological activity of steroids as determined by assay of renin substrate (hypertensinogen). Endocrinology 49: 154‐161, 1951.
 402. Helmer, O. M., and R. S. Griffith. The effect of the administration of estrogens on the renin‐substrate (hypertensinogen) content of rat plasma. Endocrinology 51: 421‐426, 1952.
 403. Helmer, O. M., and W. E. Judson. Influence of high renin substrate levels on renin‐angiotensin system in pregnancy. Am. J. Obstet. Gynecol. 99: 9‐17, 1967.
 404. Hench, P. S., E. C. Kendall, C. H. Slocum, and H. F. Polley. The effect of a hormone of the adrenal cortex (17‐hydroxy‐11‐dehydrocorticosterone: compound E) and of pituitary adrenocorticotropic hormone on rheumatoid arthritis. Proc. Staff. Meet. Mayo Clinic 24: 181‐197, 1949.
 405. Henserson, I. W., V. Jotisankasa, W. Mosley, and M. Oguri. Endocrine and environmental influences upon plasma cortisol concentrations and plasma renin activity of the eel, Anguilla anguilla L. J. Endrocrinol. 70: 81‐95, 1976.
 406. Hess, R. Arylamidase activity related to angiotensinase. Biochim. Biophys. Acta 99: 316‐324, 1965.
 407. Hessel, G. Uber renin. Klin. Wochenschr. 17: 843‐850, 1938.
 408. Hickler, R. B., D. P. Lauler, and G. W. Thorn. Plasma angiotensinase activity in patients with hypertension and edema. J. Clin. Invest. 42: 635‐648, 1963.
 409. Hirasawa, K., H. Yamamoto, A. Matsui, K. Shinozaki, S. Kobayashi, Y. Yagi, S. Morimoto, R. Takeda, and M. Murakami. The effect of mercuric chloride, of bilateral ureteral ligation and of bilateral nephrectomy on plasma renin substrate concentration in rats. Jpn. Circ. J. 32: 1591‐1595, 1968.
 410. Hirose, S., R. J. Workman, and T. Inagami. Specific antibody to hog renal renin and its application to the direct radioimmunoassay of renin in various organs. Circ. Res. 45: 275‐281, 1979.
 411. Hirose, S., H. Yokosawa, T. Inagami, and R. J. Workman. Renin and prorenin in hog brain: ubiquitous distribution and high concentration in the pituitary and pineal. Brain Res. 191: 489‐499, 1980.
 412. Hiruma, M., F. Ikemoto, and K. Yamamoto. Rat atrial natriuretic factor stimulates renin release from renal cortical slices. Eur. J. Pharmacol. 125: 151‐153, 1986.
 413. Hobart, P. M., M. Fogliano, B. A. O'Connor, I. M. Schaefer, and J. M. Chirgwin. Human renin gene: structure and sequence analysis. Proc. Natl. Acad. Sci. USA 81: 5026‐5030, 1984.
 414. Hodge, R. L., R. D. Lowe, and J. R. Vane. The effects of alteration of blood volume on the concentration of circulating angiotensin in anesthetized dogs. J. Physiol. 185: 613‐626, 1966.
 415. Hodge, R. L., K. K. F. ng, and J. R. Vane. Disappearance of angiotensin from the circulation of the dog. Nature 215: 138‐141, 1967.
 416. Hofbauer, K. G., J. Menard, J. B. Michel, and J. M. Wood. Inhibition of renin in primate Callithrix jacchus (common marmoset). Clin. Exp. Hypertens. A5: 1237‐1247, 1983.
 417. Hollenberg, N. K., W. R. Chenitz, D. F. Adams, and G. H. Williams. Reciprocal influence of salt intake on adrenal glomerulosa and renal vascular responses to angiotensin II in normal man. J. Clin. Invest. 54: 34‐42, 1974.
 418. Hollenberg, N. K., L. G. Meggs, G. H. Williams, J. Katz, J. D. Garnic, and D. P. Harrington. Sodium intake and renal responses to captopril in normal man and in essential hypertension. Kidney Int. 20: 240‐245, 1981.
 419. Hollenberg, N. K., G. H. Williams, K. J. Taub, I. Ishikawa, C. Brown, and D. F. Adams. Renal vascular response to interruption of the renin‐angiotensin system in normal man. Kidney Int. 12: 285‐293, 1977.
 420. Holm, I., R. Ollo, J.‐J. Panthier, and F. Rougeon. Evolution of aspartyl proteases by gene duplication: the mouse renin gene is organized into two homologous clusters of four exons. Eur. Mol. Biol. Org. J. 3: 557‐562, 1984.
 421. Holmes, W. N., and J. Cronshaw. Adrenal gland: some evidence for the structural and functional zonation of the steroidogenic tissues. J. Exp. Zool. 232: 627‐631, 1984.
 422. Houssay, B. A., and L. Dexter. The sensitivity to hypertensin, adrenalin and renin of unanesthetized normal, adrenalectomized, hypophysectomized and nephrectomized dogs. Ann. Intern. Med. 17: 451‐460, 1942.
 423. Howell, D. S., and J. O. Davis. Relationship of sodium retention to potassium excretion by the kidney during administration of desoxycorticosterone acetate to dogs. Am. J. Physiol. 179: 359‐363, 1954.
 424. Hsueh, W. A., E. J. Carson, and M. Israel‐Hagman. Mechanism of acid‐activation of renin: role of kallikrein in renin activation. Hypertension 3 (Suppl. I): 22‐29, 1981.
 425. Hsueh, W. A., J. A. Luetscher, E. J. Carlson, G. Grislis, E. Fraze, and A. McHargue. Changes in active and inactive renin throughout pregnancy. J. Clin. Endocrinol. Metab. 54: 1010‐1016, 1982.
 426. Hugh‐Jones, N. C., G. W. Pickering, P. H. Sanderson, H. Scarborough, and J. Vandenbroucke. The nature of the action of renin and hypertensin on renal function in the rabbit. J. Physiol. 109: 288‐307, 1949.
 427. Huidobro, F., and E. Braun‐Menendez. The secretion of renin by the intact kidney. Am. J. Physiol. 137: 47‐55, 1942.
 428. Hulthen, U. L., P. Bolli, F. W. Amann, W. Kiowski, and F. R. Buhler. Enhanced vasodilatation in essential hypertension by calcium channel blockade with verapamil. Hypertension 4 (Suppl. II): 26‐31, 1982.
 429. Hurter, R., and J. D. M. Nabarro. Aldosterone metabolism in liver disease. Acta Endocrinol. 33: 168‐174, 1960.
 430. Iana, A., D. Goldfarb, and H. Eliahou. Pressor effect of beta‐adrenergic blockade and angiotensin II in nephrectomized rats. In: Frontiers in Hypertension Research, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 440‐444.
 431. Ichikawa, I., and B. M. Brenner. Importance of efferent arteriolar vascular tone in regulation of proximal tubule fluid reabsorption and glomerulotubular balance in the rat. J. Clin. Invest. 65: 1192‐1201, 1980.
 432. Ichikawa, I., and B. M. Brenner. Glomerular action of angiotensin II. Am. J. Med. 76: 43‐49, 1984.
 433. Iimura, O., K. Shimamoto, D. Hotta, T. Nakata, T. Mito, Y. Kumamoto, K. Dempo, T. Ogihara, and K. Naruse. A case of adrenal tumor producing renin, aldosterone, and sex steroid hormones. Hypertension 8: 951‐956, 1986.
 434. Imai, T., H. Miyazaki, S. Hirose, H. Hori, T. Hayashi, R. Kageyame, H. Ohkubo, S. Nakanishi, and K. Murakami. Cloning and sequence analysis of cDNA for human renin precursor. Proc. Natl. Acad. Sci. USA 80: 7405‐7409, 1983.
 435. Inagami, T., M. Kawamura, K. Naruse, and T. Okamura. Localization of components of the renin–angiotensin system within the kidney. Federation Proc. 45: 1414‐1419, 1986.
 436. Inagami, T., and K. Murakami. Prorenin. Biomed. Res. 1: 456‐475, 1980.
 437. Iriuchijima, J. Effect of calcium antagonist nifedipine on blood pressure in various hypertensive rats. Hiroshima J. Med. Sci. 29: 15‐19, 1980.
 438. Irony, I., E. G. Biglieri, and C. E. Kater. The adrenocortical hormones in hypertensive disorders. In: Endocrine Mechanisms in Hypertension, edited by J. H. Laragh, B. M. Brenner, and N. M. Kaplan. New York: Raven, 1989, vol. 2, p. 1‐18.
 439. Ito, S., O. A. Carretero, K. Abe, W. H. Beierwaltes, and K. Yoshinaga. Effect of prostanoids on renin release from rabbit afferent arterioles with and without macula densa. Kidney Int. 35: 1138‐1144, 1989.
 440. Itoh, S., O. A. Carretero, and R. D. Murray. Possible role of adenosine in the macula densa mechanism of renin release in rabbits. J. Clin. Invest. 76: 1412‐1417, 1985.
 441. Itskovitz, H. D., S. J. Dudrick, and I. Dyrda. Plasma angiotensinase activity in hypertensive patients. Arch. Intern. Med. 119: 241‐246, 1967.
 442. Itskovitz, H. D., and L. D. Miller. Differential studies of angiotensinase activities from several tissue sources. Am. J. Med. Sci. 254: 659‐666, 1967.
 443. Itskovitz, H. D., J. J. Murphy, and H. W. Schoenberg. Differential renal function studies of the effects of angiotensin in normotensive and hypertensive patients. Am. J. Med. Sci. 253: 163‐173, 1967.
 444. Itskovitz, J., S. Rubattu, Z. Rosenwaks, H. C. Liu, N. Glorioso, L. L. Veeck, and J. E. Sealey. Prorenin in human ovarian follicular fluid (FF): correlation with oocyte‐cumulus maturity and FF steroid hormone concentrations, abstracted. Society for Gynecologic Investigation, 35th Annual Meeting. 109, 1988.
 445. Itskovitz, J., J. E. Sealey, N. Glorioso, and Z. Rosenwaks. Plasma prorenin response to hCG in ovarian hyperstimulated women: correlation with the number of ovarian follicles and steroid hormone concentrations. Proc. Natl. Acad. Sci. USA 84: 7285‐7289, 1987.
 446. Iwata, K., R. Blacher, R. L. Soffer, and C. Y. Lai. Rabbit pulmonary angiotensin‐converting enzyme: the NH2‐terminal fragment with enzymatic activity and its formation from the native enzyme by NH4‐OH treatment. Arch. Biochem. Biophys. 227: 188‐201, 1983.
 447. Jackson, B., R. B. Cubela, K. Sakaguchi, and C. I. Johnston. Characterization of angiotensin converting enzyme (ACE) in the testis and assessment of the in vivo effects of the ACE inhibitor perindopril. Endocrinology 122: 50‐55, 1988.
 448. James, G. D., J. E. Sealey, F. B. Mueller, M. H. Alderman, S. Madhavan, and J. H. Laragh. Renin relationship to sex, race, and age in a normotensive population. J. Hypertens. 4: S387‐S389, 1986.
 449. James, M. N. G., and A. R. Sielecki. Molecular structure of an aspartic proteinase zymogen, porcine pepsinogen, at 1.8‐angstrom resolution. Nature 319: 33‐38, 1986.
 450. Jard, S., B. Cantau, and K. H. Jakobs. Angiotensin II and alpha‐adrenergic agonists inhibit rat liver adenylate cyclase. J. Biol. Chem. 256: 2603‐2606, 1981.
 451. Jeunemaitre, X., J. Menard, J. Nussberger, T. T. Guyenne, H. R. Brunner, and P. Corvol. Plasma angiotensins, renin, and blood pressure during acute renin inhibition by CGP 38 560A in hypertensive patients. Am. J. Hypertens. 2: 819‐827, 1989.
 452. Johnson, J. A., J. O. Davis, and R. T. Witty. Effects of catecholamines and renal nerve stimulation on renin release in the nonfiltering kidney. Circ. Res. 29: 646‐653, 1971.
 453. Johnson, M. D., and R. L. Malvin. Stimulation of renal sodium reabsorption by angiotensin II. Am. J. Physiol. 232: F298‐F306, 1977.
 454. Johnston, C. I., J. O. Davis, F. S. Wright, and S. S. Howards. Effects of renin and ACTH on adrenal steroid secretion in the American bullfrog. Am. J. Physiol. 213: 393‐399, 1967.
 455. Johnston, C. J., and A. D. Jose. Reduced vascular response to angiotensin II in secondary hyperaldosteronism. J. Clin. Invest. 42: 1411‐1420, 1963.
 456. Jones, K. M., R. Lloyd‐Jones, A. Riondel, J. F. Tait, S. A. S. Tait, R. D. Bulbrook, and F. C. Greenwood. Aldosterone secretion and metabolism in normal man and women and in pregnancy. Acta Endocrinol. 30: 321‐342, 1959.
 457. Jones, N. F., and M. A. Barraclough. Response of the kidneys in unilateral renal artery stenosis. Lancet 1: 454‐457, 1962.
 458. Jones, N. F., M. A. Barraclough, and V. A. Perreiello. Effect of angiotensin on urea reabsorption in man. Clin. Sci. 32: 257‐269, 1967.
 459. Jonsson, O., J. Svanvik, and P. Vikgren. Regional differences in vascular tachyphylaxis to angiotensin in the cat. Angiologica 4: 299‐309, 1967.
 460. Kageyama, Y., H. Suzuki, K. Arima, and T. Saruta. Oral calcium treatment lowers blood pressure in renovascular hypertensive rats by suppressing the renin‐angiotensin system. Hypertension 10: 375‐382, 1987.
 461. Kahn, J. R., L. T. Skeggs, N. P. Shumway, and P. E. Wisenbaugh. The assay of hypertensin from the arterial blood of normotensive and hypertensive human beings. J. Exp. Med. 95: 523‐530, 1952.
 462. Kalinyak, J. E., and A. J. Perlman. Tissue‐specific regulation of angiotensinogen mRNA accumulation by dexamethasone. J. Biol. Chem. 262: 460‐464, 1987.
 463. Kaneko, Y., T. Ikeda, T. Takeda, and H. Ueda. Renin release during acute reduction of arterial pressure in normotensive subjects and patients with renovascular hypertension. J. Clin. Invest. 46: 705‐716, 1967.
 464. Kaneko, Y., J. W. McCubbin, and I. H. Page. Ability of vasoconstrictor drugs to cause adrenal medullary discharge after “sensitization” by ganglion stimulating agents. Circ. Res. 9: 1247‐1254, 1961.
 465. Kaneko, Y., T. Takeda, K. Nakasima, and H. Ueda. Effect of angiotensin on the pressor response to tyramine in normotensive subjects and hypertensive patients. Circ. Res. 19: 673‐680, 1966.
 466. Kannel, W. B., and T. Gordon. The Framingham Study: An Epidemiologic Investigation of Cardiovascular Disease. Washington, DC: U.S.D.HEW, Publ. No. 74‐618. sect. 28, 1973.
 467. Kaplan, N. M. The biosynthesis of adrenal steroids: effects of angiotensin II, adrenocorticotropin, and potassium. J. Clin. Invest. 44: 2029‐2039, 1965.
 468. Kaplan, N. M., and F. C. Bartter. The effect of ACTH, renin, angiotensin II, and various precursors on biosynthesis of aldosterone by adrenal slices. J. Clin. Invest. 41: 715‐724, 1962.
 469. Kaplan, N. M., and J. G. Silah. The effects of angiotensin II on the blood pressure in humans with hypertensive disease. J. Clin. Invest. 43: 659‐669, 1964.
 470. Kastner, P. R., J. E. Hall, and A. C. Guyton. Control of glomerular filtration rate: role of intrarenally formed angiotensin II. Am. J. Physiol. 246 (Renal Fluid Electrolyte Physiol. 15): F897‐F906, 1984.
 471. Katz, F. H., P. Romfh, and J. A. Smith. Diurnal variation of plasma aldosterone, cortisol and renin activity in supine man. J. Clin. Endocrinol. Metab. 40: 125‐134, 1975.
 472. Keeton, T. K., and W. B. Campbell. The pharmacologic alteration of renin release. Pharmacol. Rev. 32: 81‐227, 1980.
 473. Khairallah, P. A., F. M. Bumpus, I. H. Page, and R. R. Smeby. Angiotensinase with a high degree of specificity in plasma and red cells. Science 140: 672‐674, 1963.
 474. Khairallah, P. A., and I. H. Page. Mechanism of action of angiotensin and bradykinin on smooth muscle in situ. Am. J. Physiol. 200: 51‐54, 1961.
 475. Khairallah, P. A., and I. H. Page. Effect of adrenergic agents on responses of smooth muscle to angiotensin. Am. J. Physiol. 202: 841‐844, 1962.
 476. Khairallah, P. A., I. H. Page, F. M. Bumpus, and R. K. Turker. Angiotensin tachyphylaxis and its reversal. Circ. Res. 19: 247‐254, 1966.
 477. Khanum, A., and M. L. Dufau. Angiotensin II receptors and inhibitory action in Leydig cells. J. Biol. Chem. 263: 5070‐5074, 1988.
 478. Khosla, M. C., F. M. Bumpus, H. Nishimura, D. F. Opdyke, and A. Coviello. Synthesis of nonmammalian angiotensins and their comparative pressor properties in dogfish shark, domestic chicken, and rat. Hypertension 5 (Suppl. V): 22‐28, 1983.
 479. Kim, S.‐J., S. Hirose, H. Miyazaki, N. Ueno, K. Higashimori, S. Mornaga, T. Kimura, S. Sakakibara, and K. Murakami. Identification of plasma inactive renin as prorenin with a site‐directed antibody. Biochem. Biophys. Res. Commun. 126: 641‐645, 1985.
 480. Kliman, B., and R. E. Peterson. Double isotope derivative assay of aldosterone in biological extracts. J. Biol. Chem. 235: 1639‐1648, 1960.
 481. Klingbell, C. K. Corticosterone and aldosterone dose‐dependent responses to ACTH and angiotensin II in the duck (Anas platyrhynchos). Gen. Comp. Endocrinol. 59: 382‐390, 1985.
 482. Knowlton, A. I., E. N. Loeb, H. C. Stoerk, and B. C. Seegal. Development of hypertension and nephritis in normal and adrenalectomized rats treated with cortisone. Proc. Soc. Exp. Biol. Med. 72: 722‐725, 1949.
 483. Kobayashi, H., H. Uemura, and Y. Takei. Physiological role of the renin‐angiotensin system during dehydration. In: Avian Endocrinology, edited by A. Epple and M. H. Stetson. New York: Academic, 1980, p. 319‐330.
 484. Kobayashi, H., H. Uemura, Y. Takei, N. Itatsu, M. Ozawa, and K. Ichinohe. Drinking induced by angiotensin II in fishes. Gen. Comp. Endocrinol. 49: 295‐306, 1983.
 485. Kobayashi, H., H. Uemura, M. Wada, and Y. Takei. Ecological adaptation of angiotensin‐induced thirst mechanism in tetrapods. Gen. Comp. Endocrinol. 38: 93‐104, 1979.
 486. Koch‐Weser, J. Myocardial actions of angiotensin. Circ.Res. 14: 337‐344, 1964.
 487. Kokobu, T., K. Hiwada, E. Ueda, and Y. Yammura. Inhibitory effect of bile acids on renin angiotensinogen reaction system. Experientia 28: 165‐166, 1972.
 488. Kokubu, T., E. Ueda, and S. Fujimoto. Plasma angiotensinase activity in liver disease. Clin. Chim. Acta 12: 484‐488, 1965.
 489. Kokubu, T., and K. Hiwada. Human renin inhibitors. Drugs Today 23: 101‐108, 1987.
 490. Kokubu, T., K. Hiwada, E. Murakami, Y. Imamura, R. Matsueda, Y. Yabe, H. Koike, and Y. Iijima. Highly potent and specific inhibitors of human renin. Hypertension 7 (Suppl. I): 8‐11, 1985.
 491. Koletsky, S., J. M. Riviera‐Velez, and W. H. Pritchard. Production of hypertension and vascular disease by angiotensin. Arch. Pathol. 82: 99‐106, 1966.
 492. Kono, T., F. Ikeda, F. Oseko, H. Imura, and J. Endo. Suppression of captopril‐induced increase in plasma renin activity by des‐Asp1‐,Ileu8‐angiotensin II in man. J. Clin. Endocrinol. Metab. 52: 354‐358, 1981.
 493. Kopin, I. J., D. S. Goldstein, and G. Z. Feuerstein. The sympathetic nervous system and hypertension. In: Frontiers in Hypertension Research, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 283‐289.
 494. Kotchen, T. A., K. E. Krzyzaniak, J. E. Anderson, C. B. Ernst, J. H. Galla, and R. G. Luke. Inhibition of renin secretion by HCl is related to chloride in both dog and rat. Am. J. Physiol. 239 (Renal Fluid Electrolyte Physiol. 8): F44‐F49, 1980.
 495. Kowarski, S., L. A. Cowen, and D. Schacter. Decreased content of integral membrane calcium‐binding protein (IM‐CAL) in tissues of the spontaneously hyprtensive rat. Proc. Natl. Acad. Sci. USA 83: 1097‐1100, 1986.
 496. Krakoff, L. R. Measurement of plasma renin substrate by radioimmunoassay of angiotensin I: concentration in syndromes associated with steroid excess. J. Clin. Endocrinol. Metab. 37: 110‐117, 1973.
 497. Kubo, S., A. Nishioka, H. Nishimura, K. Kawamura, and T. Takatsu. Effects of captopril on arterial and venous pressure, renal function, and humoral factors in severe chronic congestive heart failure. Clin. Pharmacol. Ther. 36: 456‐463, 1984.
 498. Kuchel, O., K. Horky, M. Pazourek, and I. Gregorova. Pressor hyporeactivity to angiotensin in Addison's disease. Lancet 2: 1316‐1317, 1964.
 499. Kumamoto, K., T. A. Stewart, A. R. Johnson, and E. G. Erdos. Prolylcarboxypeptidase (angiotensinase C) in human cultured cells. J. Clin. Invest. 67: 210‐215, 1981.
 500. Kuriyama, H., Y. Itoh, H. Suzuki, A. Kitamura, and T. Itoh. Factors modifying contraction‐relaxation cycle in vascular smooth muscles. Am. J. Physiol. 243 Heart Circ. Physiol. 12): H641‐H662, 1982.
 501. Landis, E. M., H. Montgomery, and D. Sparkman. Effects of pressor drugs and of saline kidney extracts on blood pressure and skin temperature. J. Clin. Invest. 17: 189‐206, 1938.
 502. Langford, H. G. Tubular action of angiotensin. Can. Med. Assoc. J. 90: 332‐333, 1964.
 503. Langford, H. G., and F. Allison, Jr. Arteriolar changes in renin tachyphylaxis. Am. J. Physiol. 190: 130‐132, 1961.
 504. Langford, H. G., and N. Fallis. Diuretic effect of angiotensin in the chicken. Proc. Soc. Exp. Biol. Med. 123: 317‐321, 1966.
 505. Langford, H. G., and G. W. Pickering. The action of synthetic angiotensin on renal function in the unanesthetized rabbit. J. Physiol. 177: 161‐173, 1965.
 506. Lanzillo, J. J., J. Stevens, Y. Dasarathy, H. Yotsumoto, and B. L. Fanburg. Angiotensin‐converting enzymes from human tissues. Physicochemical, catalytic and immunological properties. J. Biol. Chem. 260: 14938‐14944, 1985.
 507. Laragh, J. H. The role of aldosterone in man: evidence for regulation of electrolyte balance and arterial pressure by renaladrenal system which may be involved in malignant hypertension. JAMA 174: 293‐295, 1960.
 508. Laragh, J. H. Interrelationships between angiotensin, norepinephrine, epinephrine, aldosterone secretion, and electrolyte metabolism in man. Circulation 25: 203‐211, 1962.
 509. Laragh, J. H. Hormones and pathogenesis of congestive heart failure: vasopressin, aldosterone and angiotensin II. Further evidence for renal‐adrenal interaction from studies in hypertension and cirrhosis. Circulation 25: 1015‐1023, 1962.
 510. Laragh, J. H. The mode of action and use of chlorothiazide and related compounds. Circulation 26: 122‐132, 1962.
 511. Laragh, J. H. The proper use of newer diuretics. Ann. Intern. Med. 67: 607‐613, 1967.
 512. Laragh, J. H. Vasoconstriction‐volume analysis for understanding and treating hypertension: the use of renin and aldosterone profiles. Am. J. Med. 55: 261‐274, 1973.
 513. Laragh, J. H. The renin system in high blood pressure, from disbelief to reality: converting‐enzyme blockade for analysis and treatment. Prog. Cardiovasc. Dis. 21: 159‐166, 1978.
 514. Laragh, J. H. The renin‐angiotensin‐aldosterone system for blood pressure regulation and for subdividing patients to reveal and analyze different forms of hypertension. In: Frontiers in Hypertension Research, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 183‐194.
 515. Laragh, J. H. Hypertension, vasoconstriction, and the causation of cardiovascular injury: the renin‐sodium profile as an indicator of risk. In: Frontiers of Hypertension Research, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 383‐385.
 516. Laragh, J. H. The meaning of plasma renin measurements: renin and sodium volume‐mediated (low renin) forms of vasoconstriction in experimental and human hypertension and in the oedematous states of nephrosis and heart failure. J. Hypertens. 2: S141‐S150, 1984.
 517. Laragh, J. H. Atrial natriuretic hormone, the renin‐aldosterone axis, and blood pressure‐electrolyte homeostasis. N. Engl. J. Med. 313: 1330‐1340, 1985.
 518. Laragh, J. H. The endocrine control of blood volume, blood pressure and sodium balance: atrial hormone and renin system interactions. J. Hypertens. 4 (Suppl. 5): S143‐S156, 1986.
 519. Laragh, J. H. Renovascular hypertension: a paradigm for all hypertension. J. Hypertens. 4 (Suppl. 5): S79‐S88, 1986.
 520. Laragh, J. H. Current and future directions in antihypertensive drug therapy: a special role for aldosterone antagonists. J. Drug Dev. 1 (Suppl. 2): 27‐33, 1987.
 521. Laragh, J. H. Spironolactone for Treatment of Hypertension or Congestive Heart Failure: A Review. Princeton: Excerpta Medica, 1987.
 522. Laragh, J. H. Two forms of vasoconstriction in systemic hypertension. Am. J. Cardiol. 60: 82G‐93G, 1987.
 523. Laragh, J. H. Extrarenal tissue prorenin systems do exist: are intrinsic vascular and cardiac tissue renins fact or fancy? Am. J. Hypertens. 2: 262‐265, 1989.
 524. Laragh, J. H. Issues, goals and guidelines in selecting first‐line drug therapy for hypertension. Hypertension 13 (Suppl. I): 103‐112, 1989.
 525. Laragh, J. H., M. Angers, W. G. Kelly, and S. Lieberman. Hypotensive agents and pressor substances: the effect of epinephrine, norepinephrine, angiotensin II and others on the secretory rate of aldosterone in man. JAMA 174: 234‐240, 1960.
 526. Laragh, J. H., L. Baer, H. R. Brunner, F. R. Buhler, J. E. Sealey, and E. D. Vaughan, Jr. Renin, angiotensin and aldosterone system in pathogenesis and management of hypertensive vascular disease. Am. J. Med. 52: 633‐652, 1972.
 527. Laragh, J. H., L. Baer, H. R. Brunner, F. R. Buhler, J. E. Sealey, and E. D. Vaughan, Jr. The renin‐angiotensin‐aldosterone system in the pathogenesis and management of hypertensive vascular diseases. In: Hypertension Manual, edited by J. H. Laragh. New York: Dun‐Donnelley, 1974, p. 313‐351.
 528. Laragh, J. H., P. J. Cannon, and R. P. Ames. Aldosterone secretion and various forms of hypertensive disease. Ann. Intern. Med. 59: 117‐120, 1963.
 529. Larragh, J. H., P. J. Cannon, C. J. Bentzel, A. M. Sicinski, and J. I. Meltzer. Angiotensin II, norepinephrine and the renal transport of electrolytes and water in normal man and in cirrhosis with ascites. J. Clin. Invest. 42: 1179‐1192, 1963.
 530. Laragh, J. H., P. J. Cannon, J. I. Meltzer, R. J. Fleming, and W. B. Stason. Recent advances in hypertension: combined staff clinic. Am. J. Med. 39: 616‐645, 1965.
 531. Laragh, J. H., and N. E. Capeci. Effect of administration of potassium chloride on the serum sodium and potassium concentration. Am. J. Physiol. 180: 539‐544, 1955.
 532. Laragh, J. H., D. B. Case, S. A. Atlas, and J. E. Sealey. Captopril compared with other antirenin system agents in hypertensive patients: its triphasic effects on blood pressure and its use to identify and treat the renin factor. Hypertension 2: 586‐593, 1980.
 533. Laragh, J. H., and W. G. Kelly. Aldosterone: its biochemistry and physiology. In: Advances in Metabolic Disorders, edited by R. Levine and R. Luft. New York: Academic, 1964, vol. I, p. 217‐262.
 534. Laragh, J. H., B. Lamport, J. E. Sealey, and M. H. Alderman. Diagnosis ex juvantibus: individual response patterns to drugs reveal hypertension mechanisms and simplify treatment. Hypertension 12: 223‐226, 1988.
 535. Laragh, J. H., J. G. G. Ledingham, and S. C. Sommers. Secondary aldosteronism and reduced plasma renin in hypertensive disease. Trans. Assoc. Am. Physicians 80: 168‐182, 1967.
 536. Laragh, J. H. Renin system blockade as a therapeutic strategy. Past, present, and future. Am. J. Hypertens. 4: 273S‐274S, 1991.
 537. Laragh, J. H., R. L. Letcher, and T. G. Pickering. Renin profiling for diagnosis and treatment of hypertension. JAMA 241: 151‐156, 1979.
 538. Laragh, J. H., and M. S. Pecker. Dietary sodium and essential hypertension: some myths, hopes, and truths. Ann. Intern. Med. 98: 735‐743, 1983.
 539. Laragh, J. H., and L. M. Resnick. Recognizing and treating two types of long‐term vasoconstriction in hypertension. Kidney Int. 34: S162‐S174, 1988.
 540. Laragh, J. H., and J. E. Sealey. The renin‐angiotensin‐aldosterone hormonal system and regulation of sodium, potassium, and blood pressure homeostasis. In: Handbook of Physiology. Renal Physiology, edited by J. Orloff and R. W. Berliner. Washington, DC: Am. Physiol. Soc., 1973, sect. 8, chap. 26, p. 831‐908.
 541. Laragh, J. H., and J. E. Sealey. Renin‐sodium profiling: why, how and when in clinical practice. Cardiovasc. Med. 2: 1053‐1075, 1977.
 542. Laragh, J. H., and J. E. Sealey. The renin‐angiotensin‐aldosterone system in hypertensive disorders: a key to two forms of arteriolar vasoconstriction and a possible clue to risk of vascular injury, heart attack and stroke, and prognosis. In: Hypertension, Pathophysiology, Diagnosis, and Management, edited by J. H. Laragh and B. M. Brenner. New York: Raven, 1990, p. 1329‐1348.
 543. Laragh, J. H., J. E. Sealey, and H. R. Brunner. The control of aldosterone secretion in normal and hypertensive man: abnormal renin‐aldosterone patterns in low renin hypertension. Am. J. Med. 53: 649‐663, 1972.
 544. Laragh, J. H., J. E. Sealey, and H. R. Brunner. Humoral control of renal sodium excreton. In: Modern Diuretic Therapy in the Treatment of Cardiovascular and Renal Disease (Proceedings of a symposium held at the Royal College of Physicians of London, May 8‐9, 1972), edited by A. F. Lant and G. M. Wilson. Amsterdam: Excerpta Medica, 1973, p. 26‐39.
 545. Laragh, J. H., J. E. Sealey, F. R. Buhler, E. D. Vaughan, Jr., H. R. Brunner, H. Gavras, and L. Baer. The renin axis and vasoconstriction volume analysis for understanding and treating renovascular and renal hypertension. Am. J. Med. 58: 4‐13, 1975.
 546. Laragh, J. H., J. E. Sealey, J. G. Ledingham, and M. A. Newton. Oral contraceptives: renin, aldosterone, and high blood pressure. JAMA 201: 918‐922, 1967.
 547. Laragh, J. H., J. E. Sealey, A. P. Niarchos, and T. G. Pickering. The vasoconstriction‐volume spectrum in normotension and in the pathogenesis of hypertension. Federation Proc. 41: 2415‐2423, 1982.
 548. Laragh, J. H., J. E. Sealey, and S. C. Sommers. Patterns of adrenal secretion and urinary excretion of aldosterone and plasma renin activity in normal and hypertensive subjects. Circ. Res. 18/19 (Suppl. I): 158‐174, 1966.
 549. Laragh, J. H., and H. C. Stoerk. A study of the mechanism of secretion of the sodium‐retaining hormone aldosterone. J. Clin. Invest. 36: 383‐392, 1957.
 550. Laragh, J. H., S. Ulick, V. Januszewicz, Q. B. Deming, W. G. Kelly, and S. Lieberman. Aldosterone secretion and primary and malignant hypertension. J. Clin. Invest. 39: 1091‐1106, 1960.
 551. Laragh, J. H., S. Ulick, V. Januszewicz, W. G. Kelly, and S. Lieberman. Electrolyte metabolism and aldosterone secretion in benign and malignant hypertension. Ann. Intern. Med. 53: 259‐272, 1960.
 552. Larsson, C., P. Weber, and E. Anggard. Arachidonic acid increases and indomethacin decreases plasma renin activity in the rabbit. Am. J. Pharmacol. 28: 391‐394, 1974.
 553. Laski, M. E., and N. A. Kurtzman. Characterization of acidification in the cortical and medullary collecting tubule of the rabbit. J. Clin. Invest. 72: 2050‐2059, 1983.
 554. Law, P. Y., and I. S. Edelman. Induction of citrate synthase by aldosterone in the rat kidney. J. Membr. Biol. 41: 41‐64, 1978.
 555. Leboff, M. S., R. G. Dluhy, N. K. Hollenberg, T. J. Moore, R. J. Koletsky, and G. H. Williams. Abnormal renin short feedback loop in essential hypertension is reversible with converting enzyme inhibition. J. Clin. Invest. 70: 335‐341, 1982.
 556. Leckie, B. J. Inactive renin: an attempt at a perspective. Clin. Sci. 60: 119‐130, 1981.
 557. Leckie, B. J., and N. K. McGhee. Reversible activation‐inactivation of renin in human plasma. Nature 288: 702‐704, 1980.
 558. Ledingham, J. G., M. B. Bull, and J. H. Laragh. The meaning of aldosteronism in hypertensive disease. Circ. Res. 20/21 (Suppl. II): 177‐186, 1967.
 559. Ledingham, J. G., and W. P. Leary. Catabolism of angiotensin II. In: Handbook of Experimental Pharmacology, edited by I. H. Page and F. M. Bumpus. Heidelberg: Springer, 1974, vol. 37, p. 111‐125.
 560. Lee, M. R. Renin and Hypertension: A Modern Synthesis. London: Lloyd‐Luke, Ltd., 1969.
 561. Lefer, A. M. Influence of mineralocorticoids and cations on the ionotrophic effect of angiotensin and norepinephrine in isolated cardiac muscle. Am. Heart J. 73: 674‐680, 1967.
 562. Leloir, L. F., J. M. Munoz, E. Braun‐Menendez, and J. C. Fasciolo. Secretion de renine et formation d'hypertensin. C. R. Soc. Biol. (Paris) 134: 487‐492, 1940.
 563. Lentz, K. E., L. T. Skeggs, K. R. Woods, J. R. Kahn, and N. P. Shumway. The amino acid composition of hypertensin II and its biochemical relationship to hypertensin. J. Exp. Med. 104: 183‐191, 1956.
 564. Lever, A. F. The vasa recta and countercurrent multiplication. Acta Med. Scand. 178 (Suppl. 434): 1‐43, 1965.
 565. Levitin, H., W. B. Lehman, G. Pigeon, Y. Warren, and I. S. Goldenberg. The effect of anesthesia and adrenalectomy on the renal response to angiotensin, abstracted. J. Clin. Invest. 42: 951, 1963.
 566. Lew, E. A. High blood pressure, other risk factors, and longevity: the insurance viewpoint. Am. J. Med. 55: 281‐294, 1973.
 567. Lewanczuk, R. Z., J. Wang, Z. R. Zhong, and P. K. T. Pang. Effects of spontaneous hypertensive rat plasma on blood pressure and tail artery calcium uptake in normotensive rats. Am. J. Hypertens. 2: 26‐31, 1989.
 568. Lewis, G. P., and E. Reit. The action of angiotensin and bradykinin on the superior cervical ganglion of the cat. J. Physiol. 179: 538‐553, 1965.
 569. Lewis, H. A., and H. Goldblatt. Studies on experimental hypertension. Bull. NY Acad. Med. 18: 459‐470, 1942.
 570. Leyssac, P. P., U. V. Larsen, and J. H. Thaysen. Inhibition of sodium transport in isolated renal tissue by angiotensin. Biochim. Biophys. Acta 48: 602‐605, 1961.
 571. Liebau, H., A. Distler, and H. P. Wolff. Untersuchungen zur indirekten sympathomimetischen wirkung von Angiotensin an isolierten Blutgefassen. Klin. Wochenschr. 44: 322‐326, 1966.
 572. Lieberman, J. Elevation of serum angiotensin‐converting enzyme (ACE) level in sarcoidosis. Am. J. Med. 59: 365‐372, 1975.
 573. Lin, H., and D. B. Young. Elevation of GFR by acute hyperkalemia: potential antihypertensive mechanism of potassium, abstracted. Am. J. Hypertens. 1: 73A, 1988.
 574. Lindop, G. B. M., and T. T. Downie. New morphological evidence for the synthesis and storage of renin in the human kidney: an ultrastructural immunocytochemical study. J. Hypertens. 2: 7‐10, 1984.
 575. Lippman, R. W., H. J. Ureen, and J. Oliver. Mechanism of proteinuria. IV. Effect of renin on haemoglobin excretion. J. Exp. Med. 93: 605‐614, 1951.
 576. Liu, F.‐Y., and S. G. Cogan. Angiotensin II stimulation of hydrogen ion secretion in the rat early proximal tubule: modes of action, mechanisms, and kinetics. J. Clin. Invest. 82: 601‐607, 1988.
 577. Liu, F.‐Y., and M. G. Cogan. Angiotensin II stimulates early proximal bicarbonate absorption in the rat by decreasing cyclic adenosine monophosphate. J. Clin. Invest. 84: 83‐91, 1989.
 578. Loeb, R. F. Effect of sodium chloride in treatment of patients with Addison's disease. Proc. Soc. Exp. Biol. Med. 30: 808‐812, 1933.
 579. Loudon, M., R. F. Bing, H. Thurston, and J. D. Swales. Arterial wall uptake of renal renin and blood pressure control. Hypertension 5: 629‐634, 1983.
 580. Louis, W. M., and A. E. Doyle. The effects of varying doses of angiotensin on renal function and blood pressure in man and dogs. Clin. Sci. 29: 489‐504, 1965.
 581. Loutzenhiser, R. D., and M. Epstein. Antagonists and the kidney. Am. J. Hypertens. 2: 154S‐161S, 1989.
 582. Loutzenhiser, R. D., K. Hayashi, and M. Epstein. Divergent effects of KCl‐induced depolarization on afferent and efferent arterioles. Am. J. Physiol. 257: F561‐F564, 1989.
 583. Lowitz, H. D., K. O. Stumpe, and B. Ochwadt. Micropuncture study of the action of angiotensin‐II on tubular sodium and water reabsorption in the rat. Nephron 6: 173‐187, 1969.
 584. Luetscher, J. A., Jr., and B. B. Johnson. Observations on the sodium‐retaining corticoid (aldosterone) in the urine of children and adults in relation to sodium balance and edema. J. Clin. Invest. 23: 1441‐1446, 1954.
 585. Luft, F. C., C. S. Wilcox, T. Unger, R. Kuhn, G. Demmert, P. Rohmeiss, D. Ganten, and R. B. Sterzel. Angiotensin‐induced hypertension in the rat: sympathetic nerve activity and prostaglandins. Hypertension 14: 396‐403, 1989.
 586. Lumbers, E. R. Activation of renin in human amniotic fluid by low pH. Enzymologia 40: 329‐336, 1971.
 587. Lumbers, E. R., E. K. Potter, D. I. McCloskey, M. J. Ismay, W. B. Lee, and A. D. Stevens. The effects of intravenous angiotensin II on the cardiac baroreceptor reflex. In: Frontiers in Hypertension Research, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 556‐558.
 588. Lumbers, E. R., and S. L. Skinner. Observations on the origin of renin in human urine. Circ. Res. 24: 689‐697, 1969.
 589. Lund‐Johansen, P., and P. Omvik. Hemodynamic patterns of untreated hypertensive disease. In: Hypertension: Pathophysiology, Diagnosis and Management, edited by J. H. Laragh and B. M. Brenner. New York: Raven, 1990, p. 305‐327.
 590. Luther, R. R., H. H. Stein, H. N. Glassman, and H. D. Kleinert. Renin inhibitors: specific modulators of the reninangiotensin system. Arzneimittelforschung 39: 1‐5, 1989.
 591. Lutterotti, N. V., M. J. F. Camargo, F. B. Mueller, P. B. M. W. M. Timmermans, and J. H. Laragh. Angiotensin II receptor antagonist markedly reduces mortality in salt loaded DAHLS rats. Am. J. Hypertens. 4: 346S‐349S, 1991.
 592. M'Buyamba‐Kabanga, J. R., B. Lepira, P. Lunen, K. Tshiani, R. Fagard, and A. Amery. Intracellular sodium and the response to nitrendipine or atenolol in African blacks. Hypertension 11: 100‐105, 1988.
 593. MacGregor, G. A., N. D. Markandu, S. J. Smith, and G. A. Sagnella. Does nitrendipine reveal a functional abnormality of arteriolar smooth muscle cell in essential hypertension? The effect of altering sodium balance. J. Cardiovasc. Pharmacol. 7 (Suppl. 6): S178‐S181, 1985.
 594. Mader, I. J., and L. T. Iseri. Spontaneous hypopotassemia, hypomagnesemia, alkalosis, and tetany due to hypersecretion of corticosterone‐like mineralocorticoid. Am. J. Med. 18: 976‐988, 1955.
 595. Malnic, G., R. M. Klose, and G. Giebisch. Micropuncture study of renal, potassium excretion in the rat. Am. J. Physiol. 206: 674‐686, 1964.
 596. Malnic, G., R. M. Klose, and G. Giebisch. Micropuncture study of distal tubular potassium and sodium transport in the rat nephron. Am. J. Physiol. 211: 529‐547, 1966.
 597. Malvin, R. L., D. Schiff, and S. Eiger. Angiotensin and drinking rates in the euryhaline killifish. Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R31‐R34, 1980.
 598. Marc‐Aurele, J., and M. Bergeron. Lack of evidence for an inhibitory effect of angiotensin on Na+‐K+‐adenosine triphosphatase. Rev. Can. Biol. 25: 107‐109, 1966.
 599. Marie, J., and S. Jard. Angiotensin II inhibits adenylate cyclase from adrenal cortex glomerulosa zone. FEBS Lett. 159: 97‐101, 1983.
 600. Marieb, N. J., and P. J. Mulrow. Control of aldosterone secretion in the rat, abstracted. Clin. Res. 13: 238, 1965.
 601. Marko, J., W. Hofmann, D. Goldenschmidt, and E. Ritz. Demonstration of 1,25 (OH)2 vitamin D3 receptors and actions in vascular smooth muscle cells in vitro. Calcif. Tissue Int. 41: 112‐114, 1987.
 602. Marshall, G. R., W. Vine, and P. Needleman. A specific competitive inhibitor of angiotensin II. Proc. Natl. Acad. Sci. USA 67: 1624‐1630, 1970.
 603. Marx, A. J., H. W. Deane, T. F. Mowles, and H. Sheppard. Chronic administration of angiotensin in rats: changes in blood pressure, renal and adrenal histophysiologic and aldosterone production. Endocrinology 73: 329‐337, 1963.
 604. Mason, J. C., and P. J. Hilton. Reversible renal failure due to captopril in a patient with transplant artery stenosis: case report. Hypertension 5: 623‐627, 1983.
 605. Masson, G. M. C., A. C. Corcoran, and I. H. Page. Experimental production of a syndrome resembling toxemia of pregnancy. J. Lab. Clin. Med. 38: 213‐226, 1951.
 606. Masson, G. M. C., A. C. Corcoran, and I. H. Page. Renal and vascular lesions elicited by renin in rats with desoxycorti‐costerone hypertension. Arch. Pathol. 53: 217‐225, 1952.
 607. Masson, G. M. C., C. Kashii, M. Matsunaga, and I. H. Page. Hypertensive vascular disease produced by homologous renin. Science 145: 178‐180, 1964.
 608. Masson, G. M. C., A. Mikasa, and H. Yasuda. Experimental vascular disease elicited by aldosterone and renin. Endocrinology 71: 505‐512, 1962.
 609. Masson, G. M. C., and R. H. Travis. Effects of renin on aldosterone secretion in the rat. Can. J. Physiol. Pharmacol. 46: 11‐14, 1968.
 610. McCrorey, H. L., T. Berl, T. J. Burke, A. de Torrente, and R. W. Schrier. Effect of calcium transport inhibitors on renal hemodynamics and electrolyte excretion in the dog. In: Hormonal Regulation of Sodium Excretion, edited by B. Lichardus, R. W. Schrier, and J. Ponec. New York: Elsevier/North‐Holland, 1980, p. 113‐120.
 611. McCarron, D. A., P. A. Lucas, R. S. Shneidman, and T. Druecke. Blood pressure development of the spontaneous hypertensive rat following concurrent manipulation of dietary Ca++ and Na+: relation to intestinal Ca++ fluxes. J. Clin. Invest. 76: 1147‐1154, 1985.
 612. McCubbin, J. W., R. J. Demoura, I. H. Page, and F. Olmsted. Arterial hypertension elicited by subpressor amounts of angiotensin. Science 149: 1394‐1395, 1965.
 613. McCubbin, J. W., and I. H. Page. Renal pressor system and neurogenic control of arterial pressure. Circ. Res. 12: 553‐561, 1963.
 614. McDonald, J. K., B. B. Zeitman, P. X. Callahan, and S. Ellis. Angiotensinase activity of dipeptidyl aminopeptidase I (cathepsin C) of rat liver. J. Biol. Chem. 249: 234‐240, 1974.
 615. McGiff, J. C. Natriuretic effect of angiotensin in dogs revealed after administration of reserpine and guanethidine. Circ. Res. 20: 664‐675, 1967.
 616. McGiff, J. C., K. Crowshaw, N. A. Terragno, and A. Lonigro. Renal prostaglandins: possible regulators of the renal actions of pressor hormones. Nature 227: 1255‐1257, 1970.
 617. McGiff, J. C., and T. M. Fasy. The relationship of the renal vascular activity of angiotensin II to the autonomic nervous system. J. Clin. Invest. 44: 1911‐1923, 1965.
 618. McGiff, J. C., and H. D. Itskovitz. Loss of the renal vasoconstrictor activity of angiotensin II during renal ischemia. J. Clin. Invest. 43: 2359‐2367, 1964.
 619. McGregor, D. D. The effect of sympathetic nerve stimulation on vasoconstrictor responses in perfused mesenteric blood vessels of the rat. J. Physiol. 177: 21‐30, 1965.
 620. McKenna, T. J., D. P. Island, W. E. Nicholson, and G. W. Liddle. Dopamine inhibits angiotensin stimulated aldosterone biosynthesis in bovine adrenal cells. J. Clin. Invest. 64: 287‐291, 1979.
 621. McKenzie, J. K., M. R. Lee, and W. F. Cook. Effect of hemorrhage on arterial plasma renin activity in the rabbit. Circ. Res. 19: 269‐273, 1966.
 622. Meltzer, J. I., H. J. Keim, J. H. Laragh, J. E. Sealey, K. M. Jan, and S. Chien. Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin‐sodium profiling. Ann. Intern. Med. 91: 688‐696, 1979.
 623. Menard, J., T. T. Guyenne, P. Corvol, B. Pau, D. Simon, and R. Roncucci. Direct immunometric assay of active renin in human plasma. J. Hypertens. 3 (Suppl. 3): S275‐S278, 1985.
 624. Mendelsohn, F. A., M. Dunbar, A. Allen, S. T. Chou, M. A. Millan, G. Aguilera, and K. J. Catt. Angiotensin II receptors in the kidney. Federation Proc. 45: 1420‐1425, 1986.
 625. Methot, A. L., P. Meyer, P. Biron, M. F. Lorain, G. Lagrue, and P. Milliez. Hepatic inactivation of angiotensin. Nature 203: 531‐532, 1964.
 626. Meyer, P. Similarities in cellular proliferative mechanisms in hypertension and neoplasia. In: Hypertension: Pathophysiology, Diagnosis and Management, edited by J. H. Laragh and B. M. Brenner. New York: Raven, 1990, p. 541‐545.
 627. Meyer, P., J. Menard, N. Papanicolaou, J. M. Alexandre, C. Devaux, and P. Milliez. Mechanism of renin release following furosemide diuresis in rabbit. Am. J. Physiol. 215: 908‐915, 1968.
 628. Meyer, P., B. Weil, J. Menard, J. M. Alexandre, C. Devaux, and P. Milliez. Renin stimulation mechanism in man during induced natriuresis. Rev. Can. Biol. 27: 21‐28, 1968.
 629. Michelakis, A. M., M. Caudle, and G. W. Liddle. In vitro stimulation of renin production by epinephrine, norepinephrine, and cyclic AMP. Proc. Soc. Exp. Biol. Med. 130: 748‐753, 1969.
 630. Michelakis, A. M., H. Yoshida, J. Menzie, K. Murakami, and T. Inagami. A radioimmunoassay for the direct measurement of renin in mice and its application to submaxillary gland and kidney studies. Endocrinology 94: 1101‐1105, 1974.
 631. Mitchell, K., and L. G. Navar. Superficial nephron responses to peritubular capillary infusions of angiotensins I and II. Am. J. Physiol. 252 (Renal Fluid Electrolyte Physiol. 21): F818‐F824, 1987.
 632. Miyamori, I., S. Yasuhara, Y. Takeda, H. Koshida, M. Ideka, K. Nagai, H. Okamoto, T. Morise, R. Takeda, and T. Aburano. Effects of converting enzyme inhibition on split renal function in renovascular hypertension. Hypertension 8: 415‐421, 1986.
 633. Modlinger, R. S., K. Sharif‐Zadeh, N. H. Ertel, and M. Gutkin. The circadian rhythm of renin. J. Clin. Endocrinol. Metab. 43: 1276‐1282, 1976.
 634. Moffett, R. B., R. A. McGowan, and K. W. Gross. Modulations of kidney messenger RNA levels during experimentally induced hypertension. Hypertension 8: 874‐886, 1986.
 635. Morgan, T., A. Anderson, D. Wilson, J. Myers, J. Murphy, and C. Nowson. Paradoxical effect of sodium restriction on blood pressure in people on slow‐channel blocking drugs. Lancet 1: 793, 1986.
 636. Morgan, T., and R. W. Berliner. A study by continuous microperfusion of water and electrolyte movements in the loop of Henle and distal tubule of the rat. Nephron 6: 388‐405, 1969.
 637. Morgan, T., J. Davis, and A. Gillies. Release of renin into the circulation. Kidney Int. 22 (Suppl. 12): S63‐S66, 1982.
 638. Morganti, A., J. A. Lopez‐Ovejero, T. G. Pickering, and J. H. Laragh. Role of the sympathetic nervous system in mediating the renin response to head‐up tilt: their possible synergism in defending blood pressure against postural changes during sodium deprivation. Am. J. Cardiol. 43: 600‐604, 1979.
 639. Morganti, A., J. E. Sealey, J. A. Lopez‐Ovejero, T. G. Pickering, and J. H. Laragh. The substitutive role of ACTH in supporting aldosterone response to head‐up tilt during acute renin suppression in patients with essential hypertension. Hypertension 1: 130‐135, 1979.
 640. Morris, B. J. New possibilities for intracellular renin and inactive renin now that the structure of the human renin gene has been elucidated. Clin. Sci. 71: 345‐355, 1986.
 641. Morris, B. J., J. M. Guss, W. N. Hunter, and D. F. Catanzo. A structural analysis of human renin. Clin. Exp. Pharmacol. Physiol. 12: 299‐313, 1985.
 642. Morris, B. J., H. S. Iwamoto, and I. A. Reid. Localization of angiotensinogen in rat liver by immunocytochemistry. Endocrinology 105: 796‐800, 1979.
 643. Morris, B. J., and J. E. Taylor. Activation by puff adder venom of inactive renin in normal and hypertensive rat plasma. Clin. Exp. Pharmacol. Physiol. 14: 23‐31, 1987.
 644. Motulsky, H. J., M. D. Snavely, R. J. Hughes, and P. A. Insel. Interaction of verapamil and other calcium channel blockers with alpha‐1 and alpha‐2 adrenergic receptors. Circ. Res. 52: 226‐231, 1983.
 645. Mueller, C. B., A. Surtshin, M. R. Carlin, and H. L. White. Glomerular and tubular influences on sodium and water excretion. Am. J. Physiol. 165: 411‐422, 1951.
 646. Mueller, F. B., P. Bolli, P. Erne, L. H. Block, W. Kiowski, and F. R. Buhler. Antihypertensive therapy with the longacting calcium antagonist nitrendipine. J. Cardiovasc. Pharmacol. 6 (Suppl. 7): S1073‐S1076, 1984.
 647. Mueller, F. B., J. E. Sealey, D. B. Case, S. A. Atlas, T. G. Pickering, M. S. Pecker, J. J. Preibisz, and J. H. Laragh. The captopril test for identifying renovascular disease in hypertensive patients. Am. J. Med. 80: 633‐644, 1986.
 648. Mulinos, M. G., C. L. Spingarn, and M. E. Lojkin. Diabetes insipidus‐like condition produced by small doses of desoxycorticosterone acetate in dogs. Am. J. Physiol. 135: 102‐111, 1941.
 649. Mullen, P. E., V. H. T. James, S. L. Lightman, C. Linsell, and W. S. Peart. A relationship between plasma renin activity and the rapid eye movement phase of sleep in man. J. Clin. Endocrinol. Metab. 50: 466‐469, 1980.
 650. Muller, J. Aldosterone stimulation in vitro. III. Site of action of different aldosterone‐stimulating substances on steroid biosynthesis. Acta Endocrinol. 52: 515‐526, 1966.
 651. Muller, J. Alterations of aldosterone biosynthesis of rat adrenal tissue due to increased intake of sodium and potassium. Acta Endocrinol. 58: 27‐37, 1968.
 652. Muller, J. Regulation of aldosterone biosynthesis. In: Monographs on Endocrinology, edited by F. Gross, A. Labhart, T. Mann, L. T. Samuels, and J. Zander. New York: Springer‐Verlag, vol. 5, 1971.
 653. Mullins, J. J., D. W. Burt, J. D. Windass, H. G. McTurk, and W. J. Brammar. Molecular cloning of two distinct renin genes from DBA/2 mouse. Eur. Mol. Biol. Org. J. 1: 1461‐1466, 1982.
 654. Mulrow, P. J., and W. F. Ganong. Stimulation of aldosterone secretion by angiotensin II. Yale J. Biol. Med. 33: 386‐395, 1961.
 655. Mulrow, P. J., W. F. Ganong, G. Cera, and A. Kuljian. Nature of aldosterone stimulating factor in dog kidneys. J. Clin. Invest. 41: 505‐518, 1962.
 656. Muntwyler, E., and G. E. Griffin. Creatinine clearance in normal and potassium deficient rats. Am. J. Physiol. 173: 145‐150, 1953.
 657. Murakami, E., K. Hiwada, and T. Kokubo. Effects of prostaglandins on renin substrate production by the liver. Clin. Sci. 59: 137s‐139s, 1980.
 658. Murakami, E., K. Hiwada, and T. Kokubo. Effects of insulin and glucagon on production of renin substrate by the isolated rat liver. J. Endocrinol. 85: 151‐153, 1980.
 659. Myers, B. D., W. M. Deen, and B. M. Brenner. Effects of norepinephrine and angiotensin II on the determinants of glomerular ultrafiltration and proximal tubule fluid reabsorption in the rat. Circ. Res. 37: 101‐110, 1975.
 660. Nadler, J. L., W. Hsueh, and R. Horton. Therapeutic effect of calcium channel blockade in primary aldosteronism. J. Clin. Endocrinol. Metab. 60: 896‐899, 1985.
 661. Nagatsu, I., L. Gillespie, J. E. Folk, and G. G. Glenner. Serum aminopeptidases angiotensinase and hypertension. I. Degradation of angiotensin II by human serum. Biochem. Pharmacol. 14: 721‐728, 1965.
 662. Nakane, H., Y. Nakane, P. Corvol, and J. Menard. Effect of acid, trypsin and cold treatment and of renin‐plasma interaction on the activity of renin secreted by rat kidney. Clin. Sci. 57: 233‐240, 1979.
 663. Nakano, J., and T. Kusakari. Effects of synthetic angiotensin on plasma free fatty acid and blood glucose levels. Nature 209: 922‐923, 1966.
 664. Naruse, K., Y. Takii, and T. Inagami. Immunohistochemical localizaton of renin in luteinizing hormone‐producing cells of rat pituitary. Proc. Natl. Acad. Sci. USA 78: 7579‐7583, 1981.
 665. Naruse, M. and T. Inagami. Markedly elevated specific renin levels in the adrenal in genetically hypertensive rats. Proc. Natl. Acad. Sci. USA 79: 3295‐3299, 1982.
 666. Naruse, M., C. R. Sussman, K. Naruse, R. V. Jackson, and T. Inagami. Renin exists in human adrenal tissue. J. Clin. Endocrinol. Metab. 57: 482‐487, 1983.
 667. Nasjletti, A., and G. M. C. Masson. Effects of corticosteroids on plasma angiotensinogen and renin activity. Am. J. Physiol. 217: 1396‐1400, 1969.
 668. Nasjletti, A., and G. M. C. Masson. Hepatic origin of renin substrate. Can. J. Physiol. Pharmacol. 49: 931‐932, 1971.
 669. Nasjletti, A., M. Matsunaga, and G. M. C. Masson. Effect of estrogens on pressor responses to angiotensin and renin. Proc. Soc. Exp. Biol. Med. 133: 407‐409, 1970.
 670. Navar, L. G., W. J. Champion, and C. E. Thomas. Effects of calcium channel blockade on renal vascular resistance responses to changes in perfusion pressure and angiotensin‐converting enzyme inhibition in dogs. Circ. Res. 58: 874‐881, 1986.
 671. Navar, L. G., R. A. La Grange, P. D. Bell, C. E. Thomas, and D. W. Ploth. Glomerular and renal hemodynamics during converting enzyme inhibition (SQ20,881) in the dog. Hypertension 1: 371‐377, 1979.
 672. Navar, L. G., and L. Rosivall. Contribution of the reninangiotensin system to the control of intrarenal hemodynamics. Kidney Int. 25: 857‐868, 1984.
 673. Navar, L. G., L. Rosivall, P. K. Carmines, and S. Oparil. Effects of locally formed angiotensin II on renal hemodynamics. Federation Proc. 45: 1448‐1453, 1986.
 674. Newton, M. A., and J. H. Laragh. Effects of glucocorticoid administration on aldosterone excretion and plasma renin in normal subjects, in essential hypertension and in primary aldosteronism. J. Clin. Endocrinol. Metab. 28: 1014‐1022, 1968.
 675. Newton, M. A., and J. H. Laragh. Effect of corticotropin on aldosterone excretion and plasma renin in normal subjects, in essential hypertension and in primary aldosteronism. J. Clin. Endocrinol. Metab. 28: 1006‐1013, 1968.
 676. Newton, M. A., J. E. Sealey, J. G. Ledingham, and J. H. Laragh. High blood pressure and oral contraceptives: changes in plasma renin and renin substrate and in aldosterone excretion. Am. J. Obstet. Gynecol. 101: 1037‐1045, 1968.
 677. Ng, K. K. F., and J. R. Vane. Conversion of angiotensin I to angiotensin II. Nature 215: 762‐766, 1967.
 678. Ng, K. K. F., and J. R. Vane. Fate of angiotensin I in the circulation. Nature 218: 144‐150, 1968.
 679. Nicholls, M. G., M. Tree, J. J. Brown, B. H. Douglas, R. Fraser, G. D. Hay, A. F. Lever, J. J. Morton, and J. I. S. Robertson. Angiotensin II/aldosterone dose‐response curves in the dog: effect of changes in sodium balance. Endocrinology 102: 485‐493, 1978.
 680. Nicholson, J. P., L. M. Resnick, G. D. James, R. Jennis, and J. H. Laragh. Sodium restriction and the antihypertensive effects of nitrendipine, abstracted. Clin. Res. 34: 404A, 1986.
 681. Nicholson, J. P., L. M. Resnick, and J. H. Laragh. The antihypertensive effect of verapamil at extremes of dietary sodium intake. Ann. Intern. Med. 107: 329‐334, 1987.
 682. Nicholson, J. P., L. M. Resnick, and J. H. Laragh. Hydrochlorothiazide is not additive to verapamil in treating essential hypertension. Arch. Intern. Med. 149: 125‐128, 1989.
 683. Nicholson, J. P., L. M. Resnick, T. G. Pickering, R. M. Marion, P. Sullivan, and J. H. Laragh. Relationship of blood pressure responses and the renin‐angiotensin system to first‐dose prazosin. Am. J. Med. 78: 241‐244, 1985.
 684. Nishimura, H. Comparative endocrinology of renin and angiotensin. In: The Renin—Angiotensin System, edited by J. A. Johnson and R. R. Anderson. New York: Plenum, 1980, p. 29‐77.
 685. Nishimura, H. Endocrine control of renal handling of solutes and water in vertebrates. Renal Physiol. 8: 279‐300, 1985.
 686. Nishimura, H. Evolution of the renin‐angiotensin system and its role in control of cardiovascular function in fishes. In: Evolutionary Biology of Primitive Fishes, edited by R. E. Forman, A. Gorbman, J. M. Dodd, and R. Olsson. New York: Plenum, 1985, p. 275‐293.
 687. Nishimura, H. Role of the renin‐angiotensin system in osmoregulation. In: Vertebrate Endocrinology: Fundamental and Biomedical Implications, edited by P. K. T. Pang and M. Schreibman. New York: Academic Press, 1987, vol. 2, p. 157‐187.
 688. Nishimura, H., and J. R. Bailey. Intrarenal renin‐angiotensin system in primitive vertebrates. Kidney Int. 22 (Suppl. 12): 185‐192, 1982.
 689. Nishimura, H., L. G. Lunde, and A. Zucker. Renin response to hemorrhage and hypotension in the aglomerular toadfish, Opsanus tau. Am. J. Physiol. 237 (Heart Circ. Physiol. 6): H105‐H111, 1979.
 690. Nishimura, H., M. A. Madey, and J. R. Bailey. Renin and blood pressure responses to hemorrhage and hypotensive drugs in chickens. Federation Proc. 41: 1343‐1340, 1982.
 691. Nishimura, H., and W. H. Sawyer. Vasopressor, diuretic, and natriuretic responses to angiotensin by the American eel, Anguilla rostrata. Gen. Comp. Endocrinol. 29: 337‐348, 1976.
 692. Nothstine, S. A., J. O. Davis, and R. M. Deroos. Kidney extracts and ACTH on adrenal steroid secretion in a turtle and a crocodilian. Am. J. Physiol. 221: 726‐732, 1971.
 693. Nussberger, J., D. B. Brunner, B. Waeber, and H. R. Brunner. True versus immunoreactive angiotensin II in human plasma. Hypertension 70 (Suppl. I): 1‐8, 1985.
 694. Oates, J. A., A. R. Whorton, J. F. Gerkens, R. A. Branch, J. W. Hollifield, and J. C. Frolich. The participation of prostaglandins in the control of renin release. Federation Proc. 38: 72‐74, 1979.
 695. Obana, K., M. Naruse, K. Naruse, H. Sakurai, H. Demura, T. Inagami, and K. Shizume. Synthetic rat atrial natriuretic factor inhibits in vitro and in vivo renin secretion in rats. Endocrinology 117: 1282‐1284, 1985.
 696. Odya, C. E., and E. G. Erdos. Human prolylcarboxypeptidase. Methods Enzymol. 80: 460‐466, 1981.
 697. Odya, C. E., D. Marinkovic, K. J. Hammon, T. A. Stewart, and E. G. Erdos. Purification and properties of prolylcarboxy‐peptidase (angiotensinase C) from human kidney. J. Biol. Chem. 253: 5927‐5931, 1978.
 698. Oelkers, W., J. J. Brown, R. Fraser, A. F. Lever, J. J. Morton, and J. I. S. Robertson. Sensitization of the adrenal cortex to angiotensin II in sodium deplete man. Circ. Res. 34: 69‐77, 1974.
 699. Oelkers, W., G. Schoneshofer, G. Schultze, J. J. Brown, R. Fraser, J. J. Morton, A. F. Lever, and J. I. S. Robertson. Effect of prolonged low‐dose angiotensin II infusions on the sensitivity of the adrenal cortex in man. Circ. Res. 37 (Suppl. 1): 49‐56, 1975.
 700. Ohkubo, H., R. Kageyama, M. Uhihara, T. Hirose, S. Inayama, and S. Nakashini. Cloning and sequence analysis of cDNA for rat angiotensinogen. Proc. Natl. Acad. Sci. USA 80: 2196‐2200, 1983.
 701. Ohkubo, H., K. Nakayama, T. Tanaka, and S. Nakanishi. Tissue distribution of rat angiotensinogen mRNA and structural analysis of its heterogeneity. J. Biol. Chem. 261: 319‐323, 1986.
 702. Okabe, T., M. Fujisawa, H. Yotsumoto, F. Takaku, J. J. Lanzillo, and B. L. Fanburg. Familial elevation of serum angiotensin‐converting enzyme. Q. J. Med. 55: 55‐61, 1985.
 703. Okamura, T., D. L. Clemens, and T. Inagami. Renin, angiotensins and angiotensin‐converting enzyme in neuroblastoma cells: evidence for intracellular formation of angiotensins. Proc. Natl. Acad. Sci. USA 78: 6940‐6943, 1981.
 704. Oliver, W. J., and F. Gross. Effect of testosterone and duct ligation on submaxillary renin‐like principle. Am. J. Physiol. 213: 341‐346, 1967.
 705. Oliver, W. J., R. R. Sciacca, J. Pinto, and P. J. Cannon. Participation of the prostaglandins in the control of renal blood flow during acute reduction of cardiac output in the dog. J. Clin. Invest. 67: 229‐239, 1981.
 706. Olmsted, F., and I. H. Page. Hemodynamic changes in trained dogs during experimental renal hypertension. Circ. Res. 16: 134‐139, 1965.
 707. Olmsted, F., and I. H. Page. Hemodynamic aspects of prolonged infusion of angiotensin into unanesthetized dogs. Circ. Res. 16: 140‐149, 1965.
 708. Omvik, P., E. Enger, and I. Eide. Effect of sodium depletion on plasma renin concentration before and during adrenergic beta‐receptor blockade with propranolol in normotensive man. Am. J. Med. 61: 608‐614, 1976.
 709. Ondetti, M. A., B. Rubin, and D. W. Cushman. Design of specific inhibitors of angiotensin‐converting enzyme: new class of orally effective antihypertensive agents. Science 196: 441‐444, 1977.
 710. Oparil, S., C. Vassuac, C. A. Sanders, and E. Haber. Role of renin in acute postural homeostasis. Circulation 41: 89‐95, 1970.
 711. Orr, F. R., and R. L. Filipich. Studies with angiotensin II in nephrogenic diabetes insipidus. Can. Med. Assoc. J. 97: 841‐845, 1967.
 712. Osmond, D. H., and R. M. Cooper. Cryoactivation and tryptic activation of blood “prorenin” in normal man and animals. Can. J. Physiol. Pharmacol. 56: 792‐805, 1977.
 713. Osmond, D. H., L. J. Ross, and K. D. Sciaff. Increases renin activity after cold storage of plasma. Can. J. Physiol. Pharmacol. 51: 705‐708, 1973.
 714. Osmond, D. H., R. R. Smeby, and F. M. Bumpus. Quantitative studies of renin preinhibitors and total phospholipids in organs and in plasma and erythrocyte of control, nephrectomized, and very old rats. J. Lab. Clin. Med. 73: 795‐808, 1969.
 715. Osswald, H., G. Nabakowski, and H. Hermes. Adenosine as a possible mediator of metabolic control of glomerular filtration rate. Int. J. Biochem. 12: 263‐267, 1980.
 716. Osswald, H., H. J. Schmitz, and R. Kemper. Renal action of adenosine: effect on renin secretion in the rat. Naunyn‐Schmiedebergs Arch. Pharmacol. 303: 95‐99, 1978.
 717. Padfield, P. L., and J. J. Morton. Effects of angiotensin II on arginine‐vasopressin in physiological and pathological situations in man. J. Endocrinol. 74: 251‐259, 1977.
 718. Page, I. H. On the nature of the pressor action of renin. J. Exp. Med. 70: 521‐542, 1939.
 719. Page, I. H., and O. M. Helmer. A crystalline pressor substance (angiotonin) resulting from the reaction between renin and renin activator. J. Exp. Med. 71: 29‐42, 1940.
 720. Page, I. H., and O. M. Helmer. Angiotonin activator, renin and angiotonin‐inhibitor and the mechanism of angiotonin tachyphylaxis in normal, hypertensive and nephrectomized animals. J. Exp. Med. 71: 495‐520, 1940.
 721. Page, I. H., and J. W. McCubbin. Renal vascular and systemic arterial pressure responses to nervous and chemical stimulation of the kidney. Am. J. Physiol. 173: 411‐420, 1953.
 722. Page, I. H., and J. W. McCubbin. Angiotensin. In: Renal Hypertension, edited by I. H. Page and J. W. McCubbin. Chicago: Year Book, 1968, p. 62‐98.
 723. Palaic, D. Angiotensin receptors and angiotensinase activity in vascular tissue. Trends Pharmacol. Sci. 1: 160‐161, 1980.
 724. Paller, M. S., and T. H. Hostetter. Dietary protein increases plasma renin activity and reduces pressor reactivity to angiotensin II. Am. J. Physiol. 251 (Renal Fluid Electrolyte Physiol. 20): F34‐F39, 1986.
 725. Palmore, W. P., N. J. Marieb, and P. J. Mulrow. Stimulation of aldosterone secretion by sodium depletion in nephrectomized rats. Endocrinology 84: 1342‐1351, 1969.
 726. Pals, D. T., F. D. Masucci, F. Sipos, and G. S. Denning. A specific competitive antagonist of the vascular action of angiotensin II. Circ. Res. 29: 664‐672, 1971.
 727. Pandey, K. N., M. H. Melner, M. Parmentier, and T. Inagami. Demonstration of renin activity in purified rat Leydig cells: evidence for the existence of an endogenous inactive (latent) form of enzyme. Endocrinology 115: 1753‐1759, 1984.
 728. Panisset, J. C. Effect of angiotensin on the release of acetylcholine from preganglionic and postganglionic nerve endings. Can. J. Physiol. Pharmacol. 45: 313‐317, 1967.
 729. Panisset, J. C., P. Biron, and A. Beaulnes. Effects of angiotensin on the superior cervical ganglion of the cat. Experientia 22: 394‐395, 1966.
 730. Panthier, J.‐J., I. Holm, and F. Rougeon. The mouse Rn locus: S allele of the renin regulator gene results from a single structural gene duplication. Eur. Mol. Biol. Org. J. 1: 1417‐1421, 1982.
 731. Park, C. S., and R. L. Malvin. Calcium in the control of renin release. Am. J. Physiol. 235 (Renal Fluid Electrolyte Physiol. 4): F22‐F25, 1978.
 732. Pasqualini, J. R. Aldosterone and tetrahydroaldosterone conjugation in human urine and plasma. In: Aldosterone, edited by E. E. Baulieu and P. Robel. Oxford: Blackwell, 1964, p. 131‐143.
 733. Patchett, A. A., E. Harris, E. W. Tristram, M. J. Wyvratt, M. T. Wu, D. Taub, E. R. Peterson, T. J. Ikeler, J. Ten Broecke, L. G. Payne, D. L. Ondeyka, E. D. Thorsett, W. J. Greenlee, N. S. Lohr, R. D. Hoffsommer, H. Joshua, W. V. Ruyle, J. W. Rothrock, S. D. Aster, A. L. Maycock, F. M. Robinson, R. Hirschmann, C. S. Sweet, E. H. Ulm, D. M. Gross, T. C. Vassil, and C. A. Stone. A new class of angiotensin‐converting enzyme inhibitors. Nature 288: 280‐283, 1980.
 734. Peach, M. J., F. M. Bumpus, and P. A. Khairallah. Inhibition of norepinephrine uptake in hearts by angiotensin II and analogs. J. Pharmacol. Exp. Ther. 167: 291‐299, 1969.
 735. Pelayo, J. C., and R. C. Blantz. Analysis of renal denervation in the hydropenic rat: interactions with angiotensin II. Am. J. Physiol. 246 (Renal Fluid Electrolyte Physiol. 15): F87‐F95, 1984.
 736. Peters, G. Effects of val‐5 angiotensin II‐amide and of hydrochlorothiazide on the kidneys of renal hypertensive rats. Nephron 2: 95‐106, 1965.
 737. Peterson, D. R., S. Oparil, G. Flouret, and F. A. Carone. Handling of angiotensin II and oxytocin by renal tubular segments perfused in vitro. Am. J. Physiol. 232 (Renal Fluid Electrolyte Physiol. 1): F319‐F324, 1977.
 738. Peuler, J. D., D. A. Morgan, and A. L. Mark. High calcium diet reduces blood pressure in Dahl salt‐sensitive rats by neural mechanisms. Hypertension 9 (Suppl. Ill): 159‐165, 1987.
 739. Phillips, R. A., B. J. Rolls, J. G. G. Ledingham, J. J. Morton, and M. L. Forsling. Angiotensin II‐induced thirst and vasopressin release in man. Clin. Sci. 68: 669‐674, 1985.
 740. Piccini, N., J. L. Knopf, and K. W. Gross. A DNA polymorphism, consistent with gene duplication, correlates with high renin levels in the mouse submaxillary gland. Cell 30: 205‐213, 1982.
 741. Pickel, V. M., J. Chan, and D. Ganten. Dual peroxidase and colloidal gold‐labelling study of angiotensin‐converting enzyme and angiotensin‐like immunoreactivity in the rat subfornical organ. J. Neurosci. 6: 2457‐2469, 1986.
 742. Pickens, P. T., F. M. Bumpus, A. M. Lloyd, R. R. Smeby, and I. H. Page. Measurement of renin activity in human plasma. Circ. Res. 17: 438‐448, 1965.
 743. Pickering, G. W., and M. Prinzmetal. Some observations on renin, pressor substance contained in normal kidney, together with method for its biological assay. Clin. Sci. 3: 211‐227, 1938.
 744. Pickering, G. W., and M. Prinzmetal. The effect of renin on urine formation. J. Physiol. 98: 314‐335, 1940.
 745. Pickering, T. G. Mechanisms of beta‐blockade hypotension. In: Frontiers in Hypertension Research, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 459‐461.
 746. Pickering, T. G., D. B. Case, P. A. Sullivan, and J. H. Laragh. Comparison of antihypertensive and hormonal effects of captopril and propranolol at rest and during exercise. Am. J. Cardiol. 49: 1566‐1568, 1982.
 747. Pickering, T. G., T. A. Sos, and J. H. Laragh. Role of balloon dilatation in the treatment of renovascular hypertension. Am. J. Med. 77: 61‐66, 1984.
 748. Pickering, T. G., T. A. Sos, E. D. Vaughan, Jr., D. B. Case, J. E. Sealey, G. A. Harshfield, and J. H. Laragh. Predictive value and changes of renin secretion in hypertensive patients with unilateral renovascular disease undergoing successful renal angioplasty. Am. J. Med. 76: 398‐404, 1984.
 749. Pinet, F., J. Mizrahi, I. Laboulandine, J. Menard, and P. Corvol. Regulation of prorenin secretion in cultured human transfected juxtaglomerular cells. J. Clin. Invest. 80: 724‐731, 1987.
 750. Pobiner, B. F., E. L. Hewlett, and J. C. Garrison. Role of Ni in coupling angiotensin receptors to inhibition of adenylate cyclase in hepatocytes. J. Biol. Chem. 260: 16200‐16209, 1985.
 751. Poisner, A. M., G. W. Wood, and R. Poisner. Release of inactive renin from human foetal membranes and isolate trophoblasts. Clin. Exp. Hypertens. A4: 2007‐2017, 1982.
 752. Postnov, Y. V., and S. N. Orloff. Ion transport across plasma membrane in primary hypertension. Physiol. Rev. 65: 904‐945, 1985.
 753. Poulsen, K. Kinetics of the renin system. Scand. J. Clin. Lab. Invest. 31 (Suppl. 132): 3‐86, 1973.
 754. Poulsen, K., and J. Jorgensen. An easy radioimmunological microassay of renin activity, concentration and substrate in human and animal plasma and tissues based on angiotensin I trapping by antibody. J. Clin. Endocrinol. Metab. 39: 816‐825, 1974.
 755. Poulsen, K., and E. B. Pederson. Increase in plasma renin in aggressive mice originates from kidneys, submaxillary and other salivary glands, and bites. Hypertension 5: 180‐184, 1983.
 756. Powell, J. S., J.‐P. Clozel, R. K. M. Mueller, H. Kuhn, F. Hefti, M. Hosang, and H. R. Baumgartner. Inhibitors of angiotensin‐converting enzyme prevent myointimal proliferation after vascular injury. Science 245: 186‐188, 1989.
 757. Pratt, J. H., D. A. Turner, J. A. McAteer, and D. P. Henry. Beta‐adrenergic stimulation of aldosterone production by rat adrenal capsular explants. Endocrinology 117: 1189‐1194, 1985.
 758. Pratt, R. E., J. E. Carleton, J. P. Richie, C. Heusser, and V. J. Dzau. Human renin biosynthesis and secretion in normal and ischemic kidneys. Proc. Natl. Acad. Sci. USA 84: 7837‐7840, 1987.
 759. Preibisz, J. J., J. E. Sealey, R. M. Aceto, and J. H. Laragh. Plasma renin activity measurements: an update. Cardiovasc. Rev. Rep. 3: 787‐804, 1982.
 760. Prichard, B. N. C. Hypotensive action of pronethalol. Br. Med. J. 1: 1227‐1228, 1964.
 761. Rabinowitz, L. Aldosterone and renal potassium excretion. Renal Physiol. 2: 229‐243, 1980.
 762. Ramsay, D. J. Effects of circulating angiotensin II on the brain. In: Frontiers in Neuroendocrinology, edited by W. F. Ganong and L. Martini. New York: Raven, 1982, vol. 7, p. 263‐285.
 763. Regoli, D., B. Riniker, and H. Brunner. The enzymatic degradation of various angiotensin II derivatives by serum, plasma or kidney homogenates. Biochem. Pharmacol. 12: 637‐646, 1963.
 764. Regoli, D., and J. R. Vane. A sensitive method for the assay of angiotensin. Br. J. Pharmacol. 23: 351‐359, 1964.
 765. Regoli, D., and J. R. Vane. The continuous estimation of angiotensin formed in the circulation of the dog. J. Physiol. 183: 513‐531, 1966.
 766. Reid, I. A. Action of angiotensin II on the brain: Mechanisms and physiologic role. Am. J. Physiol. 246 (Renal Fluid Electrolyte Physiol. 15): F533‐F543, 1984.
 767. Reid, I. A., W. H. Tu, K. Otsuka, T. A. Assaykeen, and W. F. Ganong. Studies concerning the regulation and importance of plasma angiotensinogen concentration in the dog. Endocrinology 93: 107‐114, 1973.
 768. Reid, W. D., and J. H. Laragh. Sodium and potassium intake, blood pressure, and pressor response to angiotensin. Proc. Soc. Exp. Biol. Med. 120: 26‐29, 1965.
 769. Reiter, M., and H. G. Schober. Oscillatorische kontraktion‐sphanomeme des Herzumuskels unter der einwirkung von Adrenalin. Arch. Exp. Pathol. Pharmacol. 250: 21‐34, 1965.
 770. Relman, A. S., and W. B. Schwartz. The effect of DOCA on electrolyte balance in normal man and its relation to sodium chloride intake. Yale J. Biol. Med. 24: 540‐558, 1952.
 771. Resink, T. J., V. A. Tkachuk, P. Erne, and F. R. Buhler. Platelet membrane Ca2+‐ATPase: blunted calmodulin‐stimulation in essential hypertension. J. Hypertens. 3 (Suppl. 3): S37‐S40, 1985.
 772. Resnick, L. M. Uniformity and diversity of calcium metabolism in hypertension: a conceptual framework. Am. J. Med. 82 (Suppl. 1B): 16‐26, 1987.
 773. Resnick, L. M., R. K. Gupta, R. E. Sosa, M. L. Corbett, J. E. Sealey, and J. H. Laragh. Effects of altered dietary calcium intake in experimental hypertension: role of intracellular free magnesium. J. Hypertens. 4 (Suppl. 5): S182‐S185, 1986.
 774. Resnick, L. M., and J. H. Laragh. Calcium metabolism and parathyroid function in primary aldosteronism. Am. J. Med. 78: 385‐390, 1985.
 775. Resnick, L. M., and J. H. Laragh. Renin, calcium metabolism and the pathophysiologic basis of antihypertensive therapy. Am. J. Cardiol. 56: 68H‐74H, 1985.
 776. Resnick, L. M., J. H. Laragh, J. E. Sealey, and M. H. Alderman. Divalent cations in essential hypertension: Relations between serum ionized calcium, magnesium, and plasma renin activity. N. Engl. J. Med. 309: 888‐891, 1983.
 777. Resnick, L. M., F. B. Mueller, and J. H. Laragh. Calcium‐regulating hormones in essential hypertension: relation to plasma renin activity and sodium metabolism. Ann. Intern. Med. 105: 649‐654, 1986.
 778. Resnick, L. M., J. P. Nicholson, and J. H. Laragh. Alterations in calcium metabolism mediate dietary salt sensitivity in essential hypertension. Trans. Assoc. Am. Physicians 98: 313‐321, 1985.
 779. Resnick, L. M., J. P. Nicholson, and J. H. Laragh. Calcium metabolism in essential hypertension: relationship to altered renin system activity. Federation Proc. 45: 2739‐2745, 1986.
 780. Resnick, L. M., J. P. Nicholson, and J. H. Laragh. Calcium, the renin‐aldosterone system, and the hypotensive response to nifedipine. Hypertension 10: 254‐258, 1987.
 781. Resnick, L. M., J. P. Nicholson, and J. H. Laragh. The antihypertensive effect of calcium channel blockade: role of sodium and calcium metabolism. J. Cardiovasc. Pharmacol. 12 (Suppl. 6): S114‐S116, 1988.
 782. Resnick, L. M., J. P. Nicholson, and J. H. Laragh. The effects of calcium channel blockade on blood pressure and calcium metabolism. Am. J. Hypertens. 2: 927‐930, 1989.
 783. Resnick, L. M., J. E. Sealey, and J. H. Laragh. Short‐ and long‐term oral calcium alters blood pressure (BP) in essential hypertension, abstracted. Federation Proc. 42: 300, 1983.
 784. Resnick, L. M., R. E. Sosa, M. L. Corbett, J. M. Gertner, J. E. Sealey, and J. H. Laragh. Effects of dietary calcium on sodium volume vs. renin‐dependent forms of experimental hypertension. Trans. Assoc. Am. Physicians 99: 172‐179, 1987.
 785. Richards, A. M., G. Tonolo, R. Fraser, J. J. Morton, B. J. Leckie, S. G. Ball, and J. I. S. Robertson. Diurnal changes in plasma atrial natriuretic factor concentrations. Clin. Sci. 73: 489‐495, 1987.
 786. Rightsel, W. A., T. Okamura, T. Inagami, J. A. Pitcock, Y. Takii, B. Brooks, P. Brown, and E. E. Muirhead. Juxtaglomerular cells grown as monolayer cell culture contain renin, angiotensin I‐converting enzyme, and angiotensins I and II/III. Circ. Res. 50: 822‐829, 1982.
 787. Robertson, P. A., and D. Rubin. Stimulation of intestinal nervous elements by angiotensin. Br. J. Pharmacol. 19: 5‐12, 1962.
 788. Robinson, B. F. Altered calcium handling as a cause of primary hypertension. Hypertension 2: 453‐460, 1984.
 789. Robinson, B. F., R. I. Dobbs, and S. Bayley. Response of forearm resistance vessels to verapamil and sodium nitroprusside in normotensive and hypertensive men: evidence for a functional abnormality of vascular smooth muscle in primary hypertension. Clin. Sci. 63: 33‐42, 1982.
 790. Rodriguez‐Puyol, D., G. Arriba, A. Blanchart, J. C. Santos, C. Caramelo, A. Fernandez‐Cruz, L. Hernando, and J. M. Lopez‐Novoa. Lack of a direct regulatory effect of atrial natriuretic factor on prostaglandins and renin release by isolated rat glomeruli. Biochem. Biophys. Res. Commun. 138: 496‐501, 1986.
 791. Rogge, J. D., A. F. Fasola, and B. Martz. Peripheral venous renin levels during +G acceleration. Aerospace Med. 38: 1024‐1028, 1967.
 792. Rosenfeld, S., R. Kraus, and A. Mccullen. Effect of renin, ischaemia and plasma protein loading on the isolated perfused kidney. Am. J. Physiol. 209: 835‐843, 1965.
 793. Rosset, E., and R. Veyrat. Inverse variations of plasma renin activity and renin substrate in normal man. Eur. J. Clin. Invest. 1: 328‐335, 1971.
 794. Rougeon, F., B. Chambraud, S. Foote, J.‐J. Panthier, R. Nageotte, and P. Corvol. Molecular cloning of a mouse submaxillary gland renin cDNA fragment. Proc. Natl. Acad. Sci. USA 78: 6367‐6371, 1981.
 795. Ruyter, J. H. C. Uber einen merkwurdigen abschnitt der vasa afferentia in der mauseniere. Histochemie 2: 242‐248, 1925.
 796. Ryan, G. B. The granulated peripolar cell epithelial cell: a potential secretory component of the renal juxtaglomerular complex. Nature 277: 655‐656, 1979.
 797. Ryan, J. W. Renin‐like enzyme in the adrenal gland. Science 158: 1589‐1590, 1967.
 798. Ryan, J. W., U. S. Ryan, D. R. Schultz, C. Whitaker, A. Chung, and F. Dorer. Subcellular localization of angiotensin‐converting enzyme (kininase II). Biochem. J. 146: 497‐499, 1975.
 799. Saint‐Andre, J.‐P., V. Rohmer, F. Alhenc‐Gelas, J. Menard, J.‐C. Bigorgne, and P. Corvol. Presence of renin, angiotensinogen, and converting enzyme in human pituitary lactotroph cells and prolactin adenomas. J. Clin. Endocrinol. Metab. 63: 231‐237, 1986.
 800. Sancho, J., R. Re, J. Burton, A. C. Barger, and E. Haber. The role of the renin‐angiotensin‐aldosterone system in cardiovascular homeostasis in normal human subjects. Circulation 50: 400‐406, 1976.
 801. Sandor, T., A. G. Fazekas, and B. H. Robinson. The biosynthesis of corticosteroids throughout the vertebrates. In: General, Comparative and Clinical Endocrinology of the Adrenal Cortex, edited by I. C. Jones and I. W. Henderson. New York: Academic, 1976, vol. 1, p. 25‐142.
 802. Schaffer, N. K., L. V. Dill, and H. J. Stander. The effect of renin on the uric acid metabolism of the pregnant and nonpregnant Dalmatian dog. Endocrinology 29: 243‐249, 1941.
 803. Schambelan, M., N. L. Brust, B. C. F. Chang, K. L. Slater, and E. G. Biglieri. Circadian rhythm and effect of posture on plasma aldosterone concentration in primary aldosteronism. J. Clin. Endocrinol. Metab. 43: 115‐131, 1976.
 804. Schmidlin, J., G. Anner, J. R. Billeter, and A. Wettstein. Uber synthesen in der Aldosteron‐Reihe I. Totalsynthese des racemischen Aldosterons. Experientia 11: 365‐368, 1955.
 805. Schneider, E. G., J. O. Davis, C. A. Robb, and J. S. Baumber. Hepatic clearance of renin in canine experimental models for low‐ and high‐output heart failure. Circ. Res. 24: 213‐219, 1969.
 806. Schnermann, J. Vascular tone as a determinant of tubuloglomerular feedback responsiveness. In: The Juxtaglomerular Apparatus and the Tubuloglomerular Feedback Mechanism, edited by A. E. G. Persson and V. Boberg. Amsterdam: Elsevier, 1988, p. 167‐176.
 807. Schnermann, J., and J. P. Briggs. Effect of angiotensin II infusion on tubuloglomerular responses, abstracted. Renal Physiol. 9: 59, 1986.
 808. Schor, N., I. Ichikawa, and B. M. Brenner. Mechanisms of action of various hormones and vasoactive substances on glomerular ultrafiltration in the rat. Kidney Int. 20: 442‐451, 1981.
 809. Schroder, R., C. Meyer‐Burgdorff, D. Rott, and O. Brahms. Vergleichende Untersuchungen uber die wirkung von A.D.H., hypertensin und renin auf die renale Wasser und elektrolyt‐Ausscheidung der Ratte. Arch. Exp. Pathol. Pharmacol. 240: 285‐312, 1961.
 810. Schuster, V. L., J. P. Kokko, and H. R. Jacobson. Angiotensin II directly stimulates transport in rabbit proximal convoluted tubules. J. Clin. Invest. 73: 507‐515, 1984.
 811. Schwartz, G. and Q. Al‐Awqati. Regulation of transepithelial H+ transport by exocytosis and endocytosis. Annu. Rev. Physiol. 48: 153‐161, 1986.
 812. Schwyzer, R., B. Iselin, H. Kappeler, B. Riniker, W. Rittel, and H. Zuber. Synthese hockwirksamer okapeptide mit der vermutlichen aminosauresequenz des noch unbekannten Hypertensins II aus Rinderserum (val 5‐Hypertensin II under val 5‐Hypertensin II‐asp‐beta‐amid). Helv. Chim. Acta 41: 1287‐1295, 1958.
 813. Scroop, G. C., and R. D. Lowe. Central pressor effect of angiotensin mediated by the parasympathetic nervous system. Nature 220: 1331‐1332, 1968.
 814. Scroop, G. C., and R. F. Whelan. A central vasomotor action of angiotensin in man. Clin. Sci. 30: 79‐90, 1966.
 815. Sealey, J. E. Measurement of the hormones of the renin system in hypertensive patients. Clin. Biochem. 14: 273‐281, 1981.
 816. Sealey, J. E. A separate prorenin–angiotensin system in reproductive and renal tissue? Evidence for renin gene expression in extrarenal vascular tissues is unconvincing. In: New Frontiers in Cardiovascular Therapy, edited by E. H. Sonnenblick, J. H. Laragh, and M. Lesch. Princeton: Excerpta Medica, 1989, p. 29‐46.
 817. Sealey, J. E., S. A. Atlas, J. H. Laragh, N. B. Oza, and J. W. Ryan. Human urinary kallikrein converts inactive to active renin and is a possible physiological activator of renin. Nature 275: 144‐145, 1978.
 818. Sealey, J. E., and S. A. Atlas. Inactive renin: speculations concerning its secretion and activation. J. Hypertens. 2 (Suppl. 1): 115‐123, 1984.
 819. Sealey, J. E., S. A. Atlas, N. Glorioso, H. Manapat, and J. H. Laragh. Cyclical secretion of prorenin during the menstrual cycle: synchronization with luteinizing hormone and progesterone. Proc. Natl. Acad. Sci. USA 82: 8705‐8709, 1985.
 820. Sealey, J. E., S. A. Atlas, and J. H. Laragh. Linking the kallikrein and renin systems via activation of inactive renin: new data and a hypothesis. Am. J. Med. 65: 994‐1000, 1978.
 821. Sealey, J. E., S. A. Atlas, and J. H. Laragh. Prorenin and other large molecular weight forms of renin. Endocrinol. Rev. 1: 365‐391, 1980.
 822. Sealey, J. E., S. A. Atlas, and J. H. Laragh. Plasma prorenin. In: Frontiers in Hypertension, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 247‐257.
 823. Sealey, J. E., S. A. Atlas, and J. H. Laragh. Plasma prorenin: physiological and biochemical characteristics. Clin. Sci. 63 (Suppl. 8): 1s‐13s, 1982.
 824. Sealey, J. E., S. A. Atlas, and J. H. Laragh. Prorenin in plasma and kidney. Federation Proc. 42: 2681‐2689, 1983.
 825. Sealey, J. E., S. A. Atlas, J. H. Laragh, M. Silverberg, and A. P. Kaplan. Initiation of plasma prorenin activation by Hageman factor‐dependent conversion of plasma prekallikrein to kallikrein. Proc. Natl. Acad. Sci. USA 76: 5914‐5918, 1979.
 826. Sealey, J. E., J. D. Blumenfeld, G. M. Bell, M. S. Pecker, S. C. Sommers, and J. H. Laragh. On the renal basis for essential hypertension: nephron heterogeneity with discordant renin secretion and sodium excretion causing a hypertensive vasoconstriction‐volume. J. Hypertens. 6: 763‐777, 1988.
 827. Sealey, J. E., F. R. Buhler, J. H. Laragh, E. L. Manning, and H. R. Brunner. Aldosterone excretion: physiological variations in man measured by radioimmunoassay or doubleisotope dilution. Circ. Res. 31: 367‐378, 1972.
 828. Sealey, J. E., F. R. Buhler, J. H. Laragh, and E. D. Vaughan, Jr. The physiology of renin secretion in essential hypertension Estimation of renin secretion rate and renal plasma flow from peripheral and renal vein renin levels. Am. J. Med. 55: 391‐401, 1973.
 829. Sealey, J. E., I. Cholst, N. Glorioso, C. Troffa, I. D. Weintraub, G. D. James, and J. H. Laragh. Sequential changes in plasma luteinizing hormone and plasma prorenin during the menstrual cycle. J. Clin. Endocrinol. Metab. 65: 1‐5, 1987.
 830. Sealey, J. E., I. Clark, M. B. Bull, and J. H. Laragh. Potassium balance and the control of renin secretion. J. Clin. Invest. 49: 2119‐2127, 1970.
 831. Sealey, J. E., J. N. Gerten, J. G. Ledingham, and J. H. Laragh. Inhibition of renin by heparin. J. Clin. Endocrinol. Metab. 27: 699‐705, 1967.
 832. Sealey, J. E., J. Gerten‐Banes, and J. H. Laragh. The renin system: variations in man measured by radioimmunoassay or bioassay. Kidney Int. 1: 240‐253, 1972.
 833. Sealey, J. E., N. Glorioso, J. Itskovitz, S. A. Atlas, T. M. Pitarresi, J. J. Preibisz, C. Troffa, and J. H. Laragh. Ovarian prorenin. Clin. Exp. Hypertens. [A]9: 1435‐1454, 1987.
 834. Sealey, J. E., N. Glorioso, J. Itskovitz, and J. H. Laragh. Prorenin as a reproductive hormone: new form of the renin system. Am. J. Med. 81: 1041‐1046, 1986.
 835. Sealey, J. E., N. Glorioso, J. Itskovitz, C. Troffa, I. Cholst, and Z. Rosenwaks. Plasma prorenin during early pregnancy: ovarian secretion under gonadotropin control. J. Hypertens. 4 (Suppl. 5): S92‐S95, 1986.
 836. Sealey, J. E., N. Glorioso, A. Toth, S. A. Atlas, and J. H. Laragh. Stimulation of plasma prorenin by gonadotropic hormones. Am. J. Obstet. Gynecol. 153: 596‐597, 1985.
 837. Sealey, J. E., M. Goldstein, T. M. Pitarresi, T. T. Kudlak, N. Glorioso, S. A. Fiamengo, and J. H. Laragh. Prorenin secretion from human testis: no evidence for secretion of active renin or angiotensinogen. J. Clin. Endocrinol. Metab. 66: 974‐978, 1988.
 838. Sealey, J. E., and J. H. Laragh. A proposed cybernetic system for sodium and potassium homeostasis: coordination of aldosterone and intrarenal physical factors. Kidney Int. 6: 281‐290, 1974.
 839. Sealey, J. E., and J. H. Laragh. Prorenin in human plasma? Methodological and physiological implications. Circ. Res. 36/37 (Suppl. 1): 10‐16, 1975.
 840. Sealey, J. E., and J. H. Laragh. Radioimmunoassay of plasma renin activity. Semin. Nucl. Med. 5: 189‐202, 1975.
 841. Sealey, J. E., D. McCord, P. A. Taufield, K. A. Ales, M. L. Druzin, S. A. Atlas, and J. H. Laragh. Plasma prorenin in first trimester pregnancy: relationship to changes in human chorionic gonadotropin. Am. J. Obstet. Gynecol. 153: 514‐519, 1985.
 842. Sealey, J. E., C. Moon, J. H. Laragh, and M. H. Alderman. Plasma prorenin: cryoactivation and relationship to renin substrate in normal subjects. Am. J. Med. 61: 731‐738, 1976.
 843. Sealey, J. E., C. Moon, J. H. Laragh, and S. A. Atlas. Plasma prorenin in normal, hypertensive, and anephric subjects and its effect on renin measurements. Circ. Res. 40 (Suppl. 1): 141‐145, 1977.
 844. Sealey, J. E., A. Overlack, J. H. Laragh, K. O. Stumpe, and S. A. Atlas. Effect of captopril and aprotonin on inactive renin. J. Clin. Endocrinol. Metab. 53: 626‐630, 1981.
 845. Sealey, J. E., R. P. White, J. H. Laragh, D. B. Case, and A. L. Rubin. Studies of plasma aldosterone in anephric people: evidence for the fundamental role of the renin system in maintaining aldosterone secretion. J. Clin. Endocrinol. Metab. 47: 52‐60, 1978.
 846. Sealey, J. E., R. P. White, J. H. Laragh, and A. L. Rubin. Plasma prorenin and renin in anephric patients. Circ. Res. 41 (Suppl. 2): 17‐21, 1977.
 847. Sealey, J. E., M. Wilson, A. Morganti, I. Zervoudakis, and J. H. Laragh. Changes in active and inactive renin throughout normal pregnancy. Clin. Exp. Hypertens. [A]4: 2373‐2384, 1982.
 848. Sellers, A. L., S. Smith, J. Marmorsten, and H. C. Goodman. Studies on the mechanism of experimental proteinuria. J. Exp. Med. 96: 643‐654, 1952.
 849. Selye, H., C. E. Hall, and E. M. Rowley. Malignant hypertension produced by treatment with desoxycorticosterone acetate and sodium chloride. Can. Med. Assoc. J. 49: 88‐92, 1943.
 850. Severs, W. B., A. E. Daniels, and J. P. Buckley. On the central hypertensive effect of angiotensin II. Int. J. Neuropharmacol. 6: 199‐205, 1967.
 851. Shingu, T., H. Matsuura, I. Inoue, A. Yuasa, M. Kusaha, and G. Kajiyama. Role of serum and intracellular ionized calcium in salt sensitivity of patients with essential hypertension, abstracted. Hypertension 14: 346, 1989.
 852. Simpson, R. U., and T. L. Goodfriend. Angiotensin and prostaglandin interactions in cultured kidney tubules. J. Lab. Clin. Med. 103: 255‐271, 1984.
 853. Simpson, S. A., J. F. Tait, A. Wettstein, R. Neher, J. Von Euw, and T. Reichstein. Isoleiurung eines neun Kristavlisierten hormons aus nebennieren mit besonders hoher wirksamkeit auf den mineralstoffwechsel. Experientia 9: 333‐335, 1953.
 854. Simpson, S. A., J. F. Tait, A. Wettstein, R. Neher, J. Von Euw, O. Schindler, and T. Reichstein. Konstitution des aldosterons des neuen mineralocorticoids. Experientia 10: 132‐133, 1954.
 855. Simpson, S. A., J. F. Tait, A. Wettstein, R. Neher, J. Von Euw, O. Shindler, and T. Reichstein. Die konstitution des aldosterons: uber Bestandteile der nebennierenrinde und verwandte stoffe. Helv. Chim. Acta 37: 1200‐1223, 1954.
 856. Singer, B., C. Losito, and S. Salmon. Some studies on the effect of angiotensin II on adrenocortical hormone secretion in hypophysectomized rats with pedicle ligation. Endocrinology 74: 325‐332, 1964.
 857. Skeggs, L. T., J. R. Kahn, K. E. Lentz, and N. P. Shumway. The preparation, purification, and amino acid sequence of a polypeptide renin substrate. J. Exp. Med. 106: 439‐453, 1957.
 858. Skeggs, L. T., W. H. Marsh, J. R. Kahn, and N. P. Shum‐way. Amino acid composition and electrophoretic properties of hypertension. J. Exp. Med. 102: 435‐440, 1955.
 859. Skeggs, L. T., Jr. Current concepts and historical perspectives of renal pressor mechanisms. J. Hypertens. 4 (Suppl. 4): S3‐S10, 1986.
 860. Skeggs, L. T., Jr., K. E. Lentz, J. R. Kahn, N. P. Shumway, and K. R. Woods. Amino acid sequence of hypertension II. J. Exp. Med. 104: 193‐197, 1956.
 861. Skeggs, L. T., Jr., W. H. Marsh, J. R. Kahn, and N. P. Shumway. The existence of two forms of hypertension. J. Exp. Med. 99: 275‐282, 1954.
 862. Skinner, S. L. Improved assay methods for renin concentration and activity in human plasma: methods using selective denaturation of renin substrate. Circ. Res. 20: 391‐402, 1967.
 863. Skinner, S. L., E. J. Cran, R. Gibson, R. Taylor, W. A. Walters, and J. J. Catt. Angiotensins I and II, active and inactive renin, renin substrate, renin activity, and angiotensinase in human liquor amnii and plasma. Am. J. Obstet. Gynecol. 121: 626‐630, 1975.
 864. Skinner, S. L., E. R. Lumbers, and E. M. Symonds. Alteration by oral contraceptives of normal menstrual changes in plasma renin activity, concentration and substrate. Clin. Sci. 36: 67‐76, 1969.
 865. Skinner, S. L., J. W. Mc Cubbin, and I. H. Page. Renal baroreceptor control of acute renin release in normotensive, nephrogenic, and neurogenic hypertensive dogs. Circ. Res. 15: 522‐531, 1963.
 866. Skott, O., and J. P. Briggs. Direct demonstration of macula densa‐mediated renin secretion. Science 237: 1618‐1620, 1987.
 867. Smeby, R. R., K. Arakawa, F. M. Bumpus, and M. M. Marsh. A proposed conformation of isoleucine angiotensin II. Biochim. Biophys. Acta 58: 550‐557, 1962.
 868. Smeby, R. R., S. Sen, and F. M. Bumpus. A naturally occurring renin inhibitor. Circ. Res. 21 (Suppl. II): 129‐133, 1967.
 869. Smith, J. B., and L. Smith. Extracellular Na+ dependence of changes in free Ca++, 45Ca++ efflux and total cell Ca++ produced by angiotensin II in cultured arterial muscle cells. J. Biol. Chem. 262: 17455‐17460, 1987.
 870. Smith, J. B., L. Smith, E. R. Brown, D. Barnes, M. A. Sabir, J. S. Davis, and R. V. Farese. Angiotensin II rapidly increases phosphatidate‐phosphoinositide synthesis, phosphoinositide hydrolysis and calcium mobilization in cultured arterial muscle cells. Proc. Natl. Acad. Sci. USA 81: 7812‐7816, 1984.
 871. Smith, S. A., B. Zacherle, T. Brown, W. G. Walker, and H. G. Langford. Effect of glomerular obstruction on renin and sodium, abstracted. In: Proc. Int. Congr. Nephrol., 4th. 1969.
 872. Smookler, H. H., W. B. Severs, W. J. Kinnard, and J. P. Buckley. Centrally mediated cardiovascular effects of angiotensin II. J. Pharmacol. Exp. Ther. 153: 485‐494, 1966.
 873. Soffer, R. L. Angiotensin‐converting enzyme. In: Biochemical Regulation of Blood Pressure, edited by R. L. Soffer. New York: John Wiley, 1981, p. 123‐164.
 874. Soffer, R. L., T. Berg, J. Sulner, and C. Y. Lai. Pulmonary and testicular angiotensin‐converting isoenzymes. Clin. Exp. Hypertens. A9: 229‐234, 1987.
 875. Soffer, R. L., and H. A. El‐Dorry. Angiotensin‐converting enzyme: some immunological, structural and developmental aspects. Federation Proc. 42: 2735‐2739, 1983.
 876. Sokabe, H., and M. Ogawa. Comparative studies of the juxtaglomerular apparatus. Int. Rev. Cytol. 37: 271‐327, 1974.
 877. Somlyo, A. V., C. Y. Woo, and A. P. Somlyo. Responses of nerve‐free vessels to vasoactive amines and polypeptides. Am. J. Physiol. 208: 748‐753, 1965.
 878. Sommers, S. C. Hypertension and kidney disease. Prog. Cardiovasc. Dis. 8: 210‐234, 1965.
 879. Sommers, S. C., A. S. Relman, and R. H. Smithwick. Histologic studies of kidney biopsy specimens from patients with hypertension. Am. J. Pathol. 34: 685‐715, 1958.
 880. Sonnenberg, H. Proximal and distal tubular function in salt‐deprived and in salt‐loaded deoxycorticosterone acetate‐escaped rats. J. Clin. Invest. 52: 263‐272, 1973.
 881. Sosa, R. E., M. Volpe, D. N. Marion, S. A. Atlas, J. H. Laragh, E. D. Vaughan, Jr., and T. Maack. Relationship between renal hemodynamic and natriuretic effects of atrial natriuretic factor. Am. J. Physiol. 250 (Renal Fluid Electrolyte Physiol. 19): F520‐F524, 1986.
 882. Soubrier, F., F. Alhenc‐Gelas, C. Hubert, J. Allegrini, M. John, G. Tregear, and P. Corvol. Two putative active centers in human angiotensin I‐converting enzyme revealed by molecular cloning. Proc. Natl. Acad. Sci. USA 85: 9386‐9390, 1988.
 883. Soubrier, F., J. J. Panthier, P. Corvol, and F. Rougeon. Molecular cloning and nucleotide sequence of a human renin cDNA fragment. Nucleic Acids Res. 11: 7181‐7190, 1983.
 884. Sowers, J. R., G. Berg, V. S. Martin, and D. M. Mayes. Dopaminergic modulation of aldosterone secretion in the rhesus monkey: evidence that dopamine effects the late pathway of aldosterone biosynthesis by inhibiting the conversion of corticosterone to 18‐hydroxycorticosterone. Endocrinology 110: 1173‐1177, 1982.
 885. St. Clair, D. K., K. A. Presper, P. L. Smith, D. C. Stump, and E. C. Heath. Bovine angiotensin‐converting enzyme: amino‐terminal sequence analysis and preliminary characterization of a hybridization‐selected primary translation product. Biochem. Biophys. Res. Commun. 141: 968‐972, 1986.
 886. Stachenko, J., and C. J. P. Giroud. Functional zonation of the adrenal cortex: site of ACTH action. Endocrinology 64: 743‐752, 1959.
 887. Stahl, J., H. Jahn, P. Reville, T. Kurtz, and F. Kuntzman. Suppression by spirolactones of the natriuretic effect of angiotensin peculiar to certain cirrhotics. C. R. Acad. Sci. [III] 261: 5247‐5249, 1965.
 888. Stallone, J. N., and H. Nishimura. Angiotensin II (All)‐induced natriuresis in anesthetized domestic fowl. Federation Proc. 44: 1364‐1360, 1985.
 889. Steiger, M., and T. Reichstein. Desoxy‐corticosteron (21‐oxy‐progesteron) aus‐delta 5‐3‐oxy‐atiocholensaure. Helv. Chim. Acta 20: 1164‐1179, 1937.
 890. Stein, J. H., R. Osgood, S. Boonjarern, and T. Ferris. A comparison of the segmental analysis of sodium reabsorption during Ringer's and hyperoncotic albumin infusion in the rat. J. Clin. Invest. 52: 2313‐2323, 1973.
 891. Stephens, G. A., and J. A. Creekmore. Response of plasma renin activity to hypotension and angiotensin converting enzyme inhibitor in the turtle. J. Comp. Physiol. [B] 154: 287‐294, 1984.
 892. Stier, C. G., I. F. Benter, S. Ahmad, H. Zuo, N. Selig, S. Roethel, S. Levine, and H. D. Itskovitz. Enalapril prevents stroke and kidney dysfunctions in salt loaded stroke prone spontaneously hypertensive rats. Hypertension 13 (2): 115‐121, 1989.
 893. Stockigt, J. R., R. D. Collins, and E. G. Biglieri. Determination of plasma renin concentration by angiotensin I immunoassay. Circ. Res. 28/29 (Suppl. II): 175‐189, 1971.
 894. Stoerk, H. C., J. H. Laragh, R. M. Aceto, and T. Budzilovich. Edema and ascites following the ligation of both ureters in rats. Am. J. Pathol. 58: 51‐67, 1970.
 895. Stone, D. K., D. W. Seldin, J. P. Kokko, and H. R. Jacobsen. Mineralocorticoid modulation of rabbit medullary collecting duct acidification. J. Clin. Invest. 72: 77‐83, 1983.
 896. Streeten, D. H. P., G. H. Anderson, Jr., and T. G. Dalakos. Angiotensin blockade: its clinical significance. Am. J. Med. 60: 817‐824, 1976.
 897. Strittmatter, S. M., E. A. Thiele, M. S. Kapiloff, and S. H. Snyder. A rat brain isozyme of angiotensin‐converting enzyme. Unique specificity for amidated peptide substrates. J. Biol. Chem. 260: 9825‐9832, 1985.
 898. Stumpe, K. O., R. Kolloch, H. Vetter, W. Gramann, F. Kruck, C. Ressel, and M. Higuchi. Acute and long‐term studies of the mechanisms of action of beta‐blocking drugs in lowering blood pressure. Am. J. Med. 60: 853‐865, 1976.
 899. Swales, J. D., and A. M. Heagerty. Vascular renin‐angiotensin system: the unanswered questions. J. Hypertens. 5 (Suppl. 2): S1‐S5, 1987.
 900. Tagawa, H., and A. J. Vander. Effects of adenosine compounds on renal function and renin secretion in dogs. Circ. Res. 26: 327‐338, 1970.
 901. Tait, J. F., S. A. S. Tait, B. Little, and K. R. Laumas. The disappearance of 7‐H3‐d‐aldosterone in the plasma of normal subjects. J. Clin. Invest. 40: 72‐80, 1961.
 902. Talledo, O. E. Renin‐angiotensin system. II. Inactivation of angiotensin in normal pregnancy. Am. J. Obstet. Gynecol. 97: 571‐572, 1967.
 903. Taugner, R., E. Hackenthal, R. Nobiling, M. Harlacher, and G. Reb. The distribution of renin in the different segments of the renal arterial tree. Histochemistry 73: 75‐88, 1981.
 904. Taugner, R., E. Hackenthal, E. Rix, R. Nobiling, and K. Poulsen. Immunocytochemistry of the renin‐angiotensin system: renin, angiotensin, angiotensin II, and converting enzyme in the kidneys of mice, rats, and tree shrews. Kidney Int. 12 (Suppl.): S33‐S43, 1982.
 905. Taylor, A. A., J. O. Davis, and B. Braverman. Deoxycorticosterone secretion in the bullfrog: effects of ACTH, hypophysectomy, and renin. Am. J. Physiol. 223: 858‐863, 1972.
 906. Tewksbury, D. A., and R. A. Dart. Elevated high molecular weight angiotensinogen levels in hypertensive pregnant women. Hypertension 4: 729‐734, 1982.
 907. Tewksbury, D. A., R. A. Dart, and J. Travis. The amino terminal amino acid sequence of human angiotensinogen. Biochem. Biophys. Res. Commun. 99: 1311‐1315, 1981.
 908. Tewksbury, D. A., W. L. Frome, and M. L. Dumas. Characterization of human angiotensinogen. J. Biol. Chem. 253: 3817‐3820, 1978.
 909. Tewksbury, D. A., E. S. Tryon, R. E. Burrill, and R. A. Dart. High molecular weight angiotensinogen: a pregnancy associated protein. Clin. Chim. Acta 158: 7‐12, 1986.
 910. Thames, M. D. Renin release: reflex control and adrenergic mechanisms. J. Hypertens. 2 (Suppl. 1): 57‐66, 1984.
 911. Thoenen, H., A. Hurlimann, and W. Hafely. Effect of angiotensin on response to postganglionic sympathetic stimulation of the cat spleen: lack of facilitation of norepinephrine liberation. Med. Pharmacol. Exp. 13: 379‐387, 1965.
 912. Thorn, G. W., R. P. Howard, K. Emerson, and W. M. Firor. Treatment of Addison's disease with pellets of crystalline adrenal cortical hormone (synthetic desoxycorticosterone acetate) implanted subcutaneously. Bull. Johns Hopkins Hosp. 64: 339‐365, 1939.
 913. Thurau, K. Renal hemodynamics. Am. J. Med. 36: 698‐719, 1964.
 914. Thurau, K. Influence of sodium concentration at macula densacells on tubular sodium load. Ann. NY Acad. Sci. 139: 388‐399, 1966.
 915. Tigerstedt, R., and P. G. Bergman. Niere und Kreislauf. Skand. Arch. Physiol. 8: 223‐271, 1998.
 916. Timmermans, P. B. M. W. M., D. J. Carini, A. T. Chiu, J. V. Duncia, W. A. Price, Jr., G. J. Wells, P. C. Wong, R. R. Wexler, and A. L. Johnson. The discovery and physiological effects of a new class of highly specific angiotensin II‐receptor antagonists. In: Hypertension: Pathophysiology, Diagnosis and Management, edited by J. H. Laragh and B. M. Brenner. New York: Raven, 1990, p. 2351‐2360.
 917. Timmermans, P. B. M. W. M., M. J. Mathy, M. J. M. C. Thoolen, A. de Jonge, B. Wilffert, and P. A. Van Zweiten. Invariable susceptibility to blockade by nifedipine of vasoconstriction to various alpha‐2 adrenoceptor agonists in pithed rats. J. Pharm. Pharmacol. 36: 772‐775, 1984.
 918. Timmermans, P. B. M. W. M., M. J. Mathy, B. Wilffert, H. O. Kalkman, M. J. Thoolen, A. de Jonge, J. C. Van Meel and P. A. Van Zweiten. Differential effect of calcium entry blockers on alpha‐1‐adrenoceptor‐mediated vasoconstriction in vivo. Naunyn‐Schmiedebergs Arch. Pharmacol. 324: 239‐245, 1983.
 919. Tobian, L. J. Interrelationship of electrolytes, juxtaglomerular cells and hypertension. Physiol. Rev. 40: 280‐312, 1960.
 920. Tobian, L. J. Renin release and its role in renal function and the control of salt balance and arterial pressure. Federation Proc. 26: 48‐54, 1967.
 921. Tobian, L. J., K. Coffee, and P. McCrea. Contrasting exchangeable sodium in rats with different types of Goldblatt hypertension. Am. J. Physiol. 217: 458‐460, 1969.
 922. Tobian, L. J., and P. Nason. The augmentation of proteinuria after acute sodium depletion in the rat. J. Lab. Clin. Med. 67: 224‐228, 1966.
 923. Tobian, L. J., J. Thompson, R. Twedt, and J. Janecek. The granulation of juxtaglomerular cells in renal hypertension, desoxycorticosterone and postdesoxycorticosterone hypertension, adrenal regeneration hypertension, and adrenal insufficiency. J. Clin. Invest. 37: 660‐671, 1958.
 924. Tobian, L. J., A. Tomboulian, and J. Janecek. The effect of high perfusion pressures on the granulation of juxtaglomerular cells in an isolated kidney. J. Clin. Invest. 38: 605‐611, 1959.
 925. Troffa, C., N. Glorioso, P. Christofalo, and S. A. Atlas. Stimulation of plasma inactive renin by dexamethasone in the cat, abstracted. The Endocrine Society, 68th Meeting, 678, 1986, p. 200.
 926. Tucci, J. R., E. A. Espiner, P. I. Jagger, G. L. Pauk, and D. P. Lauler. ACTH stimulation of aldosterone secretion in normal subjects and in patients with chronic adrenocortical insufficiency. J. Clin. Endocrinol. 27: 568‐575, 1967.
 927. Turgeon, C., and S. C. Sommers. Juxtaglomerular cell counts and human hypertension. Am. J. Pathol. 38: 227‐241, 1961.
 928. Ueda, H., Y. Kaneko, T. Takeda, T. Ikeda, and S. Yagi. Observations on the mechanism of renin release by hydralazine in hypertensive patients. Circ. Res. 26/27 (Suppl. II): 201‐206, 1970.
 929. Ulick, S. Stereospecificity in the metabolism of aldosterone in man. J. Biol. Chem. 236: 680‐684, 1961.
 930. Ulick, S., J. H. Laragh, and S. Lieberman. The isolation of a urinary metabolite of aldosterone and its use to measure the rate of secretion of aldosterone by the adrenal ortex of man. Trans. Assoc. Am. Physicians 71: 225‐235, 1958.
 931. Ulick, S., and S. Lieberman. Evidence for the occurrence of a metabolite of aldosterone in urine. J. Am. Chem. Soc. 79: 6567‐6568, 1957.
 932. Ulick, S., and K. K. Vetter. Simultaneous measurement of secretory rates of aldosterone and 18‐hydroxycorticosterone. J. Clin. Endocrinol. 25: 1015‐1026, 1965.
 933. Ulick, S., K. K. Vetter, and J. T. August. Identification of two C18‐oxygenated corticosteroids isolated from human urine. J. Biol. Chem 237: 3364‐3374, 1962.
 934. Urquhart, J., J. O. Davis, and J. T. Higgins, Jr. Effects of prolonged infusion of angiotensin II in normal dogs. Am. J. Physiol. 205: 1241‐1246, 1963.
 935. Usberti, M., G. Di Minno, B. Ungaro, B. Cianciaruso, S. Federico, G. Ardillo, A. Gargiulo, F. Martucci, M. Pannain, A. M. Cerbone, G. Conte, C. Pecoraro, and V. E. Andreucci. Angiotensin II inhibition with captopril on plasma ADH, PG synthesis, and renal function in humans. Am. J. Physiol. 250 (Renal Fluid Electrolyte Physiol. 19): F986‐F990, 1986.
 936. Vagnucci, A. I., D. P. Lauler, R. B. Hickler, and G. W. Thorn. Acute infusion of synthetic angiotensin II in patients with essential hypertension: its effect on renal hemodynamics and on electrolyte and water excretion. Circulation 29: 523‐532, 1964.
 937. Van Breeman, C., P. Leijten, H. Yamamoto, P. Aaronson, and C. Cauvin. Ca2+ activation of vascular smooth muscle. Hypertension 8 (Suppl. II): 89‐95, 1986.
 938. Van Zweiten, P. A., J. C. A. Van Meel, and P. B. M. W. M. Timmermans. Pharmacology of calcium entry blockers in interaction with vascular alpha‐adrenoceptors. Hypertension 5 (Suppl. II): 3‐17, 1983.
 939. Vander, A. J. Inhibition of distal tubular sodium reabsorption by angiotensin II. Am. J. Physiol. 205: 133‐138, 1963.
 940. Vander, A. J. Effect of catecholamines and the renal nerves on renin secretion in anesthetized dogs. Am. J. Physiol. 209: 659‐662, 1965.
 941. Vander, A. J. Control of renin release. Physiol. Rev. 47: 359‐382, 1967.
 942. Vander, A. J. Direct effects of prostaglandin on renal function and renin release in anesthetized dog. Am. J. Physiol. 214: 218‐221, 1968.
 943. Vander, A. J. Inhibition of renin release in the dog by vasopressin and vasotocin. Circ. Res. 23: 605‐609, 1968.
 944. Vander, A. J. Direct effects of potassium on renin secretion and renal function. Am. J. Physiol. 219: 455‐459, 1970.
 945. Vander, A. J., and J. Carlson. Mechanism of the effects of furosemide on renin secretion in anesthetized dogs. Circ. Res. 25: 145‐152, 1969.
 946. Vander, A. J., and G. W. Geelhoed. Inhibition of renin secretion by angiotensin II. Proc. Soc. Exp. Biol. Med. 120: 399‐403, 1965.
 947. Vander, A. J., and J. R. Luciano. Effects of mercurial diuresis and acute salt depletion on renin release in dog. Am. J. Physiol. 212: 651‐656, 1967.
 948. Vander, A. J., and R. Miller. Control of renin secretion in the anesthetized dog. Am. J. Physiol. 207: 537‐546, 1964.
 949. Vane, J. R. The release and fate of vasoactive hormones in the circulation. Br. J. Pharmacol. 35: 209‐242, 1969.
 950. Vaughan, E. D., Jr., F. R. Buhler, J. H. Laragh, J. E. Sealey, L. Baer, and R. H. Bard. Renovascular hypertension: renin measurements to indicate hypersecretion and contralateral suppression, estimate renal plasma flow, and score for surgical curability. Am. J. Med. 55: 402‐414, 1973.
 951. Vaughan, E. D., Jr., J. H. Laragh, I. Gavras, F. R. Buhler, H. Gavras, H. R. Brunner, and L. Baer. Volume factor in low and normal renin essential hypertension treatment with either spironolactone of chlorthalidone. Am. J. Cardiol. 32: 523‐532, 1973.
 952. Velletri, P. A., D. R. Aquilano, E. Bruckwick, C. H. Tsai‐Morris, M. L. Dufau, and W. Lovenberg. Endocrinological control and cellular localization of rat testicular angiotensin‐converting enzyme. Endocrinology 116: 2516‐2522, 1985.
 953. Velletri, P. A., M. L. Billingsley, and W. Lovenberg. Angiotensin‐converting enzyme isozymes: effects of chelators and CoC12. Biochim. Biophys. Acta 839: 71‐82, 1985.
 954. Venning, E. H., I. Dyrenfurth, and J. C. Beck. Effect of corticotropin and prednisone on the excretion of aldosterone in man. J. Clin. Endocrinol. Metab. 16: 1541‐1553, 1956.
 955. Vetter, H., W. Vetter, C. Warnholz, J. M. Bayer, H. Kaser, and K. Vielhaber. Renin and aldosterone secretion in pheochromocytoma. Am. J. Med. 60: 866‐871, 1976.
 956. Villareal, H., H. Arcila, J. Diaz, and P. Sierra. Effect of angiotensin on renal transport of sodium in renovascular hypertension. Am. J. Cardiol. 19: 793‐796, 1967.
 957. Villareal, H., H. Arcila, J. Diaz, and P. Sierra. Effect of angiotensin on the renal transport of sodium in essential hypertension. Circulation 35: 889‐894, 1967.
 958. Villareal, H., J. Nieto de Pascual, H. Arcila, C. Lopez‐Viva, and P. Sierra. The action of angiotensin on renal transport of sodium in the dog. Nephron 1: 338‐347, 1964.
 959. Volhard, F., and T. Fahr. Die Brightsche Nierenkranheit: Klinik, Pathologie und Atlas. Berlin: Springer, 1914.
 960. Volpe, M., G. Odell, H. D. Kleinert, M. J. F. Camargo, J. H. Laragh, J. A. Lewicki, T. Maack, E. D. Vaughan, Jr., and S. A. Atlas. Antihypertensive and aldosterone‐lowering effects of synthetic atrial natriuretic factor in renin‐dependent renovascular atrial natriuretic factor in renin‐dependent renovascular hypertension. J. Hypertens. 2 (Suppl. 3): 313‐315, 1984.
 961. Waite, M. A. Measurement of concentrations of angiotensin I in human blood by radioimmunoassay. Clin. Sci. Mol. Med. 45: 51‐64, 1973.
 962. Wallia, R., A. Greenberg, and J. B. Puschett. Renal hemodynamic and tubular transport effects of nitrendipine. J. Lab. Clin. Med. 105: 498‐503, 1985.
 963. Warren, A. Y., D. J. Craven, and E. M. Symonds. Production of active and inactive renin by cultured explants from human female genital tract. Br. J. Obstet. Gynaecol. 89: 628‐632, 1982.
 964. Waugh, W. H. Angiotensin II: local renal effects of physiological increments in concentration. Can. J. Physiol. Pharmacol. 50: 711‐716, 1972.
 965. Weinberger, M. H., N. J. Kramer, C. E. Grim, and L. P. Peterson. The effect of posture and saline loading on plasma renin activity and aldosterone concentration in pregnant, nonpregnant and estrogen treated women. J. Clin. Endocrinol. Metab. 44: 69‐77, 1977.
 966. Weinberger, M. H., M. B. Wade, W. Aoi, T. Usa, M. Dentino, F. Luft, and C. E. Grim. An extra‐renal source of “renin‐like” activity in anephric man. Circ. Res. 40 (Suppl. I): 1‐4, 1977.
 967. Weiner, M. W., E. J. Weinman, M. Kashgarian, and J. P. Hayslett. Accelerated reabsorption in the proximal tubule produced by volume depletion. J. Clin. Invest. 50: 1379‐1385, 1971.
 968. Wenting, G. J., H. L. Tan Tjiong, F. H. M. Derkx, J. H. B. Debruyn, A. J. Man In't Veld, and M. A. D. H. Schalekamp. Split renal function after captopril in unilateral renal artery stenosis. Br. Med. J. 288: 886‐890, 1984.
 969. Wesson, L. G. Glomerular and tubular factors in the renal excretion of sodium chloride. Medicine 36: 281‐396, 1957.
 970. Westfall, T. C., and M. J. Peach. Action of angiotensin on myocardial and renal catecholamines in the rabbit. Biochem. Pharmacol. 14: 1916‐1920, 1965.
 971. White, P. C., M. I. New, and B. Dupont. Congenital adrenal hyperplasia. N. Engl. J. Med. 316: 1519‐1524, 1987.
 972. Whitebread, S. M. Mele, B. Kamber, and M. Degasparo. Preliminary biochemical characterization of two angiotensin II receptor sub‐types. Biochem. Biophys. Res. Commun. 163: 284‐291, 1989.
 973. Wigger, H. J., and S. A. Stalcup. Distribution and development of angiotensin‐converting enzyme in the fetal and newborn rabbit: An immunofluorescence study. Lab. Invest. 38: 581‐585, 1978.
 974. Williams, G. H., N. K. Hollenberg, T. J. Moore, R. G. Dluhy, S. Z. Bavli, H. S. Solomon, and J. H. Mersey. Failure of renin suppression by angiotensin II in hypertension. Circ. Res. 42: 46‐52, 1978.
 975. Wilson, C., and G. W. Pickering. Acute arterial lesions in rabbits with experimental renal hypertension. Clin. Sci. 3: 343‐355, 1938.
 976. Wilson, J. X., and D. G. Butler. 6‐Hydroxydopamine treatment diminishes noradrenergic and pressor responses to angiotensin II in adrenalectomized ducks. Endocrinology 112: 653‐658, 1983.
 977. Wilson, M., A. Morganti, I. Zervoudakis, R. L. Letcher, B. M. Romney, P. Von Oeyon, S. Papera, J. E. Sealey, and J. H. Laragh. Blood pressure, the renin‐aldosterone system and sex steroids throughout normal pregnancy. Am. J. Med. 68: 97‐104, 1980.
 978. Wilson, S. K., and R. H. Heptinstall. Effects of acute, angiotensin‐induced hypertension on intrarenal arteries in the rat. Kidney Int. 25: 492‐501, 1984.
 979. Winternitz, M. C, E. Mylon, L. L. Waters et al. Studies on the relation of the kidney to cardiovascular disease. Yale J. Biol. Med. 12: 623‐680, 1940.
 980. Wisgerhof, M., and R. D. Brown. Increased adrenal sensitivity to angiotensin II in low renin essential hypertension. J. Clin. Invest. 61: 1456‐1462, 1978.
 981. Wolfe, L. K., R. D. Gordon, D. P. Island, and G. W. Liddle. An analysis of factors determining the circadian pattern of aldosterone secretion. J. Clin. Endocrinol. 26: 1261‐1266, 1966.
 982. Wong, P. C., T. M. Reilly, and P. B. M. W. M. Timmermans. Effect of a monoclonal antibody to angiotensin II on hemodynamic responses to noradrenergic stimulation in pithed rats. Hypertension 14: 488‐497, 1989.
 983. Wood, J. E. Peripheral venous and arteriolar responses to infusions of angiotensin in normal and hypertensive subjects. Circ. Res. 9: 768‐774, 1961.
 984. Woodcock, E. A., and C. I. Johnston. Inhibition of adenylate cyclase by angiotensin II in rat renal cortex. Endocrinology 111: 1687‐1691, 1982.
 985. Woods, L. L., H. L. Mizelle, J.‐P. Montani, and J. E. Hall. Mechanisms controlling renal hemodynamics and electrolyte excretion during amino acids. Am. J. Physiol. 251 (Renal Fluid Electrolyte Physiol. 20): F303‐F312, 1986.
 986. Woods, R. I., W. P. Anderson, and P. I. Korner. Renal and systemic effects of enalapril in chronic one‐kidney hypertension. Hypertension 8: 109‐116, 1986.
 987. Wright, F. S., N. Strieder, N. B. Fowler, and G. Giebisch. Potassium secretion by distal tubule after potassium adaptation. Am. J. Physiol. 221: 437‐448, 1971.
 988. Yamamoto, T., M. Shimizu, M. Morioka, M. Kitano, H. Wakabayashi, and N. Aizawa. Role of angiotensin II in the pathogenesis of hyperdipsia in chronic renal failure. JAMA 256: 604‐608, 1986.
 989. Yang, H.‐Y. T., E. G. Erdos, and Y. Levin. A dipeptidyl carboxypeptidase that converts angiotensin I and inactivates bradykinin. Biochim. Biophys. Acta 214: 374‐377, 1970.
 990. Yang, H.‐Y. T., and N. H. Neff. Distribution and properties of angiotensin‐converting enzyme of rat brain. J. Neurochem. 19: 2443‐2450, 1972.
 991. Yang, R. H., H. Jin, Y.‐F. Chen, S. Oparil, and J. M. Wyss. Dietary calcium supplementation prevents the exaggerated responsiveness of anterior hypothalamic alpha‐adrenoreceptors to NaCl‐loaded spontaneous hypertensive rats. J. Cardiovasc. Pharmacol. 13: 162‐167, 1989.
 992. Yokosawa, H., N. Yokosawa, and T. Inagami. Specific antibody to human renal renin and its cross‐reactivity with inactive human plasma prorenin. Proc. Soc. Exp. Biol. Med. 164: 466‐470, 1980.
 993. Young, D. B. Comparison of a beta‐blocker and converting enzyme inhibitor in two types of experimental hypertension. In: Frontiers in Hypertension Research, edited by J. H. Laragh, F. R. Buhler, and D. W. Seldin. New York: Springer‐Verlag, 1981, p. 436‐439.
 994. Young, D. B., and T. E. Jackson. Effects of aldosterone on potassium distribution. Am. J. Physiol. 243 (Regulatory Integrative Comp. Physiol. 12): R526‐R530, 1982.
 995. Young, D. B., R. E. McCaa, Y. J. Pan, and C. Guyton. The natriuretic and hypotensive effects of potassium. Circ. Res. 38 (Suppl. II): 84‐89, 1976.
 996. Yu, R., and C. J. Dickinson. Neurogenic effects of angiotensin. Lancet 2: 1276, 1965.
 997. Yusuf, S., R. Peto, J. Lewis, R. Collins, and P. Sleight. Beta blockade during and after myocardial infarction: an overview of the randomized trials. Prog. Cardiovasc. Dis. 28: 335‐371, 1985.
 998. Zabludowski, J., S. Clark, S. G. Ball, A. J. Brown, G. C. Inglis, and A. F. Lever. Pressor effects of brief and prolonged infusions of epinephrine in the conscious rat. Am. J. Physiol. 246 (Heart Circ. Physiol. 15): H683‐H689, 1984.
 999. Zachariah, P. K., G. L. Schwartz, S. G. Ritter, and C. G. Strong. Plasma predictors of calcium channel blocker efficacy in hypertension. J. Cardiovasc. Pharmacol. 1990 (In press).
 1000. Zambraski, E. J., and C. D. Ciccone. Alpha adrenergic activity and renal function in two‐kidney, deoxycorticosterone acetate hypertensive swine. Drug Dev. Res. 2: 275‐281, 1982.
 1001. Zehr, J. E. Control of renin by reflex mechanisms in man and experimental animals. J. Hypertens. 2 (Suppl. 1): 49‐56, 1984.
 1002. Zehr, J. E., K. D. Kurz, A. A. Seymour, and H. D. Schultz. Mechanisms controlling renin release. In: The Renin‐Angiotensin System, edited by J. A. Johnson and R. R. Anderson. New York: Plenum, 1980, p. 135‐170.
 1003. Zemel, M. B., S. M. Gualdoni, and J. R. Sowers. Sodium excretion and plasma renin activity in normotensive and hypertensive black adults is affected by dietary calcium and sodium. J. Hypertens. 4 (Suppl. 6): 5343‐5345, 1986.
 1004. Zemel, M. B., S. M. Gualdoni, M. F. Walsh, P. Komanicky, P. Standley, D. Johnson, W. Fetter, and J. R. Sowers. Effects of sodium and calcium on calcium metabolism and blood pressure regulation in hypertensive black adults. J. Hypertens. 4 (Suppl. 5): 5364‐5366, 1986.
 1005. Ziegler, M., and F. Gross. Effect of blood volume on renin‐like activity in blood. Can. Med. Assoc. J. 116: 774‐778, 1964.
 1006. Zimmerman, B. G. Effect of acute sympathectomy on responses to angiotensin and norepinephrine. Circ. Res. 11: 780‐787, 1962.
 1007. Zimmerman, B. G., F. M. Abboud, and J. W. Eckstein. Effects of norepinephrine and angiotensin on total and venous resistance in the kidney. Am. J. Physiol. 206: 701‐706, 1964.
 1008. Zimmerman, B. G., and L. Whitmore. Effect of angiotensin and phenoxybenzamine on release of norepinephrine in vessels during sympathetic nerve stimulation. J. Neuropharmacol. 6: 27‐38, 1967.
 1009. Zipser, R. D., J. C. Hoefs, P. F. Speckart, P. K. Zea, and R. Heston. Prostaglandins: modulators of renal function and pressor resistance in chronic liver disease. J. Clin. Endocrinol. Metab. 48: 895‐900, 1979.

Contact Editor

Submit a note to the editor about this article by filling in the form below.

* Required Field

Article Title: Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis
 

How to Cite

John H. Laragh, Jean E. Sealey. Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis. Compr Physiol 2011, Supplement 25: Handbook of Physiology, Renal Physiology: 1409-1541. First published in print 1992. doi: 10.1002/cphy.cp080231