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Control of Sodium Excretion: An Integrative Approach

Franklyn G. Knox, Joey P. Granger

10.1002/cphy.cp080121

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 Intrarenal Hemodynamic Control of Sodium Excretion
1.1 Effects of Peritubular Starling Forces on Sodium Excretion
1.2 Effects of Medullary Blood Flow on Sodium Excretion
1.3 Effects of Renal Perfusion Pressure on Sodium Excretion
2 Neural Control of Sodium Excretion
2.1 Sodium Intake and Body Fluid Volumes
2.2 Low‐Pressure Baroreceptors
2.3 Renal Sympathetic Nerve Activity
3 Hormonal Control of Sodium Excretion
3.1 Renin–Angiotensin–Aldosterone System
3.2 Renal Prostaglandin System
3.3 Renal Kallikrein–Kinin System
3.4 Natriuretic Hormone
3.5 Atrial Natriuretic Peptide
4 Summary
Figure 1. Figure 1.

Effect of intrarenal albumin infusion on proximal reabsorption of sodium in extracellular fluid volume‐expanded dogs (left column) and hydropenic dogs (right column).

Adapted from Ott et al. 234
Figure 2. Figure 2.

Effects of intrarenal prostaglandin E2 infusion with (open bar) or without (solid bar) renal interstitial hydrostatic pressure (RIHP) increases and a prostaglandin analogue (PA) (hatched bar) on renal blood flow and fractional sodium excretion.

Adapted from Haas et al. 117
Figure 3. Figure 3.

Relationship between fractional excretion of sodium (FENa) and renal subcapsular pressure (Psc) in rats with (open circles) or without (closed circles) ligated renal lymphatics during normal (A) and volume‐expanded (B) conditions.

Adapted from Wilcox et al. 298
Figure 4. Figure 4.

Representation of proximal tubule cell in relation to peritubular capillary under normal and volume‐expanded conditions. Sodium diffuses down electrochemical concentration gradient from tubule lumen into cell and then is actively transported into interstitial space, with water following passively. Uptake of this reabsorbate from interstitial space into peritubular capillary is determined by balance of Starling forces across capillary wall, where πc and πi represent oncotic pressures and Pc and Pi represent hydrostatic pressures in the peritubular capillary and interstitium, respectively. In response to volume expansion, a new balance of Starling forces is achieved where Pc is elevated and πc is reduced. These changes result in a reduction in uptake of reabsorbate, thereby increasing renal interstitial volume and Pi and reducing πi. The resultant increase in Pi leads to a greater backleak of sodium from paracellular space into tubule lumen, thereby reducing net sodium reabsorption.
Figure 5. Figure 5.

Pathway whereby increases in medullary blood flow increase sodium excretion.
Figure 6. Figure 6.

Effects of renal perfusion pressure on sodium excretion, glomerular filtration rate (GFR), and renal blood flow (RBF).

Adapted from Baer et al. 8
Figure 7. Figure 7.

Pathways whereby increases in renal perfusion pressure increase sodium excretion.
Figure 8. Figure 8.

Effects of renal perfusion pressure on fractional sodium excretion in normal dogs and in dogs pretreated with a prostaglandin synthesis inhibitor, indomethacin.

Adapted from Carmines et al. 46
Figure 9. Figure 9.

Fractional reabsorption of sodium (FRNa) from proximal tubules of deep (lower right panel) and superficial (upper right panel) nephrons and whole kidney (left panel) in response to increases in renal perfusion pressure (RPP).

Adapted from Haas et al. 115
Figure 10. Figure 10.

Effects of aldosterone infusion on mean arterial pressure, cumulative sodium balance, and urinary sodium excretion in dogs when renal perfusion pressure was permitted to increase (left) and when renal perfusion pressure was servocontrolled at normal levels (right).

Adapted from Hall et al. 122
Figure 11. Figure 11.

Pathway whereby renal sympathetic nervous system increases sodium reabsorption in response to extracellular fluid volume contraction.
Figure 12. Figure 12.

Effects of changes in sodium space on blood volume of conscious anephric dogs. Each point represents mean values from dogs in 10% saline infusion group (squares), 5% saline infusion group (triangles), and in control group with no infusion (circles). Solid line has been drawn through mean values of blood volume and sodium space measured at 20 min, 40 min, 1 h, 2 h, 3 h, 4 h, and 5 h after infusion.

Adapted from Manning and Guyton 193
Figure 13. Figure 13.

Sodium excretion of bilaterally denervated (closed circles) and control (open circles) conscious rats during normal‐, low‐ and high‐sodium diet.

Adapted from Bencsáth et al. 23
Figure 14. Figure 14.

Cumulative sodium balance in renal innervated (solid circles) and bilaterally renal denervated (open circles) rats on normal‐ and low‐sodium diet.

Adapted from DiBona and Sawin 69
Figure 15. Figure 15.

Sodium excretory response to saline expansion in normal humans and in humans pretreated with metoclopramide.

Adapted from Krishna et al. 175
Figure 16. Figure 16.

Pathways whereby the renin–angiotensin‐aldosterone system increases sodium reabsorption in response to extracellular fluid volume contraction.
Figure 17. Figure 17.

Effects of sodium depletion on papillary plasma flow (PPF), urine osmolality, and papillary tip sodium content and osmolality.

Adapted from Chou et al. 54
Figure 18. Figure 18.

Effects of peritubular infusion of angiotension II on steady‐state sodium concentration gradient (ΔCNa) across proximal tubule wall. Open circles, angiotensin II; closed circles, control.
Figure 19. Figure 19.

Changes in sodium excretion during increasing rates of angiotensin infusion with renal arterial pressure either maintained at control level (servocontrol; open circles) or permitted to increase (normal; closed circles).

Adapted from Olsen et al. 227
Figure 20. Figure 20.

Intrarenal efects of angiotensin II antagonist on renal hemodynamics and sodium and water excretion, in sodium‐depleted dogs. Open bars, saline; closed bars, antagonist.

Adapted from Hall et al. 120
Figure 21. Figure 21.

Pathway whereby renal prostaglandin system increases sodium excretion in response to extracellular fluid volume expansion.
Figure 22. Figure 22.

Changes in renal function produced by increasing rates of sodium arachidonate in normal dogs (solid circles) and in dogs pretreated with prostaglandin synthesis inhibitor (open circles).

Adapted from Tannenbaum et al. 284
Figure 23. Figure 23.

Effects of vehicle (V) or meclofenamate (M) administration on sodium excretion after load of 77 mEq sodium chloride in normal dogs.

Adapted from Altsheler et al. 3
Figure 24. Figure 24.

Pathway whereby renal kallikrein–kinin system increases sodium excretion in response to extracellular volume expansion.
Figure 25. Figure 25.

Effects of intrarenal infusion of bradykinin for 60 min on glomerular filtration rate, renal blood flow, and sodium excretion.

Adapted from Granger and Hall 108
Figure 26. Figure 26.

Pathway whereby atrial natriuretic peptide system increases sodium excretion in response to extracellular fluid volume expansion.
Figure 27. Figure 27.

Effect of graded constriction of pulmonary artery on plasma atrial natriuretic peptide (ANP) concentration and relationship between change in right atrial pressure (RAP), left atrial pressure (LAP), and plasma ANP.

Adapted from Metzler et al. 210
Figure 28. Figure 28.

Effect of intrarenal infusion of synthetic atrial natriuretic peptide on renal function and renin release. Open bars, control; closed bars, atrial natriuretic peptide; hatched bars, recovery. MAP, mean arterial pressure; FF, filtration fraction; , fractional phosphate excretion; RBF, renal blood flow; V, urinary flow rate; FEPO fractional lithium excretion; GFR, glomerular filtration rate; FENa, fractional sodium excretion, Uosmol, urine osmolality; RVR, renal vascular resistance; FEK, fractional potassium excretion; RSR, renin secretion rate.

Adapted from Burnett et al. 39
Figure 29. Figure 29.

Effect of intrarenal infusion of atrial natriuretic peptide at rate that does not increase glomerular filtration rate on fractional excretion of sodium and lithium.

Adapted from Salazar et al. 251
Figure 30. Figure 30.

Effect of atrial natriuretic peptide on sodium influx into exponential growing cells. Atrial natriuretic peptide was added for 30 min, and 2‐min 22Na + uptakes were measured.
Figure 31. Figure 31.

Effects of acute atrial appendectomy (ATRX) on plasma atrial natriuretic peptide and renal response to acute saline load.

Adapted from Schwab et al. 260
Figure 32. Figure 32.

Effects of acute saline load on plasma atrial natriuretic peptide (ANP) concentration and plasma renin activity (PRA) in conscious dogs.

Adapted from Salazar et al. 254
Figure 33. Figure 33.

Effects of progressive increments of sodium intake by continuous intravenous saline infusion on plasma levels of atrial natriuretic peptide (ANP).

Adapted from Salazar et al. 252
Figure 34. Figure 34.

Temporal changes in plasma levels of atrial natriuretic peptide (ANP), cumulative sodium balance, and sodium excretion during aldosterone escape.

Adapted from Granger et al. 110
Figure 35. Figure 35.

Effects of left atrial (LA) stretch on urine volume, sodium excretion, potassium excretion, and plasma atrial natriuretic factor (ANF) in normal and cardiac‐denervated dogs.

Adapted from Goetz et al. 102


Figure 1.

Effect of intrarenal albumin infusion on proximal reabsorption of sodium in extracellular fluid volume‐expanded dogs (left column) and hydropenic dogs (right column).

Adapted from Ott et al. 234


Figure 2.

Effects of intrarenal prostaglandin E2 infusion with (open bar) or without (solid bar) renal interstitial hydrostatic pressure (RIHP) increases and a prostaglandin analogue (PA) (hatched bar) on renal blood flow and fractional sodium excretion.

Adapted from Haas et al. 117


Figure 3.

Relationship between fractional excretion of sodium (FENa) and renal subcapsular pressure (Psc) in rats with (open circles) or without (closed circles) ligated renal lymphatics during normal (A) and volume‐expanded (B) conditions.

Adapted from Wilcox et al. 298


Figure 4.

Representation of proximal tubule cell in relation to peritubular capillary under normal and volume‐expanded conditions. Sodium diffuses down electrochemical concentration gradient from tubule lumen into cell and then is actively transported into interstitial space, with water following passively. Uptake of this reabsorbate from interstitial space into peritubular capillary is determined by balance of Starling forces across capillary wall, where πc and πi represent oncotic pressures and Pc and Pi represent hydrostatic pressures in the peritubular capillary and interstitium, respectively. In response to volume expansion, a new balance of Starling forces is achieved where Pc is elevated and πc is reduced. These changes result in a reduction in uptake of reabsorbate, thereby increasing renal interstitial volume and Pi and reducing πi. The resultant increase in Pi leads to a greater backleak of sodium from paracellular space into tubule lumen, thereby reducing net sodium reabsorption.



Figure 5.

Pathway whereby increases in medullary blood flow increase sodium excretion.



Figure 6.

Effects of renal perfusion pressure on sodium excretion, glomerular filtration rate (GFR), and renal blood flow (RBF).

Adapted from Baer et al. 8


Figure 7.

Pathways whereby increases in renal perfusion pressure increase sodium excretion.



Figure 8.

Effects of renal perfusion pressure on fractional sodium excretion in normal dogs and in dogs pretreated with a prostaglandin synthesis inhibitor, indomethacin.

Adapted from Carmines et al. 46


Figure 9.

Fractional reabsorption of sodium (FRNa) from proximal tubules of deep (lower right panel) and superficial (upper right panel) nephrons and whole kidney (left panel) in response to increases in renal perfusion pressure (RPP).

Adapted from Haas et al. 115


Figure 10.

Effects of aldosterone infusion on mean arterial pressure, cumulative sodium balance, and urinary sodium excretion in dogs when renal perfusion pressure was permitted to increase (left) and when renal perfusion pressure was servocontrolled at normal levels (right).

Adapted from Hall et al. 122


Figure 11.

Pathway whereby renal sympathetic nervous system increases sodium reabsorption in response to extracellular fluid volume contraction.



Figure 12.

Effects of changes in sodium space on blood volume of conscious anephric dogs. Each point represents mean values from dogs in 10% saline infusion group (squares), 5% saline infusion group (triangles), and in control group with no infusion (circles). Solid line has been drawn through mean values of blood volume and sodium space measured at 20 min, 40 min, 1 h, 2 h, 3 h, 4 h, and 5 h after infusion.

Adapted from Manning and Guyton 193


Figure 13.

Sodium excretion of bilaterally denervated (closed circles) and control (open circles) conscious rats during normal‐, low‐ and high‐sodium diet.

Adapted from Bencsáth et al. 23


Figure 14.

Cumulative sodium balance in renal innervated (solid circles) and bilaterally renal denervated (open circles) rats on normal‐ and low‐sodium diet.

Adapted from DiBona and Sawin 69


Figure 15.

Sodium excretory response to saline expansion in normal humans and in humans pretreated with metoclopramide.

Adapted from Krishna et al. 175


Figure 16.

Pathways whereby the renin–angiotensin‐aldosterone system increases sodium reabsorption in response to extracellular fluid volume contraction.



Figure 17.

Effects of sodium depletion on papillary plasma flow (PPF), urine osmolality, and papillary tip sodium content and osmolality.

Adapted from Chou et al. 54


Figure 18.

Effects of peritubular infusion of angiotension II on steady‐state sodium concentration gradient (ΔCNa) across proximal tubule wall. Open circles, angiotensin II; closed circles, control.



Figure 19.

Changes in sodium excretion during increasing rates of angiotensin infusion with renal arterial pressure either maintained at control level (servocontrol; open circles) or permitted to increase (normal; closed circles).

Adapted from Olsen et al. 227


Figure 20.

Intrarenal efects of angiotensin II antagonist on renal hemodynamics and sodium and water excretion, in sodium‐depleted dogs. Open bars, saline; closed bars, antagonist.

Adapted from Hall et al. 120


Figure 21.

Pathway whereby renal prostaglandin system increases sodium excretion in response to extracellular fluid volume expansion.



Figure 22.

Changes in renal function produced by increasing rates of sodium arachidonate in normal dogs (solid circles) and in dogs pretreated with prostaglandin synthesis inhibitor (open circles).

Adapted from Tannenbaum et al. 284


Figure 23.

Effects of vehicle (V) or meclofenamate (M) administration on sodium excretion after load of 77 mEq sodium chloride in normal dogs.

Adapted from Altsheler et al. 3


Figure 24.

Pathway whereby renal kallikrein–kinin system increases sodium excretion in response to extracellular volume expansion.



Figure 25.

Effects of intrarenal infusion of bradykinin for 60 min on glomerular filtration rate, renal blood flow, and sodium excretion.

Adapted from Granger and Hall 108


Figure 26.

Pathway whereby atrial natriuretic peptide system increases sodium excretion in response to extracellular fluid volume expansion.



Figure 27.

Effect of graded constriction of pulmonary artery on plasma atrial natriuretic peptide (ANP) concentration and relationship between change in right atrial pressure (RAP), left atrial pressure (LAP), and plasma ANP.

Adapted from Metzler et al. 210


Figure 28.

Effect of intrarenal infusion of synthetic atrial natriuretic peptide on renal function and renin release. Open bars, control; closed bars, atrial natriuretic peptide; hatched bars, recovery. MAP, mean arterial pressure; FF, filtration fraction; , fractional phosphate excretion; RBF, renal blood flow; V, urinary flow rate; FEPO fractional lithium excretion; GFR, glomerular filtration rate; FENa, fractional sodium excretion, Uosmol, urine osmolality; RVR, renal vascular resistance; FEK, fractional potassium excretion; RSR, renin secretion rate.

Adapted from Burnett et al. 39


Figure 29.

Effect of intrarenal infusion of atrial natriuretic peptide at rate that does not increase glomerular filtration rate on fractional excretion of sodium and lithium.

Adapted from Salazar et al. 251


Figure 30.

Effect of atrial natriuretic peptide on sodium influx into exponential growing cells. Atrial natriuretic peptide was added for 30 min, and 2‐min 22Na + uptakes were measured.



Figure 31.

Effects of acute atrial appendectomy (ATRX) on plasma atrial natriuretic peptide and renal response to acute saline load.

Adapted from Schwab et al. 260


Figure 32.

Effects of acute saline load on plasma atrial natriuretic peptide (ANP) concentration and plasma renin activity (PRA) in conscious dogs.

Adapted from Salazar et al. 254


Figure 33.

Effects of progressive increments of sodium intake by continuous intravenous saline infusion on plasma levels of atrial natriuretic peptide (ANP).

Adapted from Salazar et al. 252


Figure 34.

Temporal changes in plasma levels of atrial natriuretic peptide (ANP), cumulative sodium balance, and sodium excretion during aldosterone escape.

Adapted from Granger et al. 110


Figure 35.

Effects of left atrial (LA) stretch on urine volume, sodium excretion, potassium excretion, and plasma atrial natriuretic factor (ANF) in normal and cardiac‐denervated dogs.

Adapted from Goetz et al. 102
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Article Title: Control of Sodium Excretion: An Integrative Approach
 

How to Cite

Franklyn G. Knox, Joey P. Granger. Control of Sodium Excretion: An Integrative Approach. Compr Physiol 2011, Supplement 25: Handbook of Physiology, Renal Physiology: 927-967. First published in print 1992. doi: 10.1002/cphy.cp080121