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Corticosteroids and the Kidney

Diana Marver

10.1002/cphy.cp080232

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 Role of the Receptor
1.2 Transport and Biochemical Studies: Toad Bladder
1.3 Transport and Biochemical Studies: Mammalian Kidney
2 Renal Corticosteroid Receptor Distribution
3 Mineralocorticoid Action
3.1 Regulation of Na+ Absorption and K+ Secretion: Cortical Collecting Tubule
3.2 Other Target Sites That May Regulate Na+ and/or K+
3.3 Acid Excretion
3.4 Mineralocorticoid Escape
4 Glucocorticoid Action
4.1 GFR/RBF: K+ Excretion
4.2 Metabolism: Gluconeogenesis and Ammoniagenesis
4.3 Acid Excretion
4.4 Calcium Excretion
4.5 Concentration/Dilurion Urine
Figure 1. Figure 1.

Aldosterone‐stimulated short‐circuit current (SCC) in toad bladder. Aldosterone (0.28 μM) or diluent was added to serosal surface of paired bladders obtained from toads soaked 3–5 days in either water or saline. Diminished response in toads soaked for long periods in saline as seen in this study has been noted by others 225.

from Crabbe 35
Figure 2. Figure 2.

Influence of amphotericin B on short‐circuit current (SCC) in toad bladder compared to that of vasopressin. When amphotericin B was added to apical membrane, a rapid rise in SCC occurred that was not augmented by subsequent addition of vasopressin (solid line). Amphotericin B addition after vasopressin, however, enhanced SCC beyond that seen with vasopressin alone.

From Lichenstein and Leaf 157
Figure 3. Figure 3.

Schematic of relative nuclear versus cytoplasmic labeling of [3H]aldosterone and [3H]SC 26304, a spirolactone. After the portal vein and hepatic artery were ligated, adrenalectomized rats were injected IV with either [3H]aldosterone or [3H]SC 26304 and the kidneys removed 2 or 10 min later. Nonspecific binding was determined in rats injected with [3H]steroid and a 100‐fold excess of unlabeled D‐aldosterone. Scale at left is in terms of mol × 10−14/mg protein. The results show that even though cytoplasmic labeling of mineralocorticoid receptors with [3H]SC 26304 exceeds that of [3H]aldosterone, only [3H]aldosterone‐receptor complexes are retained by nuclear chromatin. Furthermore, the absolute amount of [3H]aldosterone retained at 10 min exceeded that at 2 min, despite the fact that cytoplasmic labeling was significantly reduced because of the corresponding fall in plasma levels of [3H]steroid.

Adapted from Marver et al. 172
Figure 4. Figure 4.

Relative specific binding of three corticosteroids along the adrenalectomized rat or rabbit nephron. Binding activity was determined using either in vivo administration of [3H]dexamethasone and subsequent autoradiography of tissue segments, or in vitro binding assays with isolated segments and either [3H]aldosterone or [3H]corticosterone. Aldosterone and dexamethasone studies utilized rabbits; corticosterone studies, rats.

Adapted from the studies of Doucet and Katz 47, Farman et al. 69, Lee et al. 154
Figure 5. Figure 5.

Relationship between steady‐state plasma aldosterone concentration and flux of sodium and potassium in rabbit cortical collecting tubule. Closed circles represent the lumen‐to‐bath 22Na tracer flux; open circles represent net K+ transport determined on luminal samples monitoring perfused and collected K+ concentrations. There was no significant difference in bath‐to‐lumen tracer 22Na flux measured in several groups having both high and low plasma aldosterone levels. Overall average was 1.4 pEq/cm‐s, and group averages ranged from 1.0 to 1.7 pEq/cm‐s.

adapted from the study of Schwartz and Burg 216
Figure 6. Figure 6.

Influence of aldosterone on electrolyte handling by adrenalectomized rat: inhibition of the response by actinomycin D. Animals were adrenalectomized 24 h prior to the study and maintained on 0.035 M NaCl drinking water without food. They were given diluent (control) or aldosterone (1 μg/kg BW loading dose +1 μg/kg/h infusion) ± 300 μg/kg actinomycin D. Some controls received only actinomycin D. Shown at the top are plasma Na+ and K+ concentrations as a function of time following initiation of study. At the bottom is shown either fractional excretion of Na+ (FE Na) or urinary excretion of K+ (UKV).

From Horisberger and Diezi 118
Figure 7. Figure 7.

Influence of aldosterone on CCD Na+,K+‐ATPase activity. Upper panel: Na+,K+‐ATPase activities in mol/kg dry tubule wt/h at 37°C in CCDs obtained from normal (NORM) rabbits are denoted by the solid bar (±SEM). Stippled bars include activities seen in CCDs from adrenalectomized (ADX) rabbits injected at time 0 with diluent or 10 μg/kg BW aldosterone (ALDO) ± the spirolactone SC 26304 (SPIRO), or 100 μg‐kg BW dexamethasone (DEX) and sacrificed at either 1.5 or 3 h. Bottom panel: Na+,K+‐ATPase activities at 3 h postinjection of: (1) diluent (ADX); (2) 10 μg‐kg BW aldosterone (ALDO); or (3) 10μg/kg BW aldosterone + a total of 5 mg/kg BW amiloride (AMIL) given in four split doses, starting at t= −30 min.

Adapted from Petty et al. 195
Figure 8. Figure 8.

Influence of corticosteroid therapy on transepithelial voltage (Vte) and the voltage across the apical (Va) and basolateral (Vb) membrane of the cortical collecting tubule principal cell. Rabbits were treated with DOCA (2 mg/kg/day) or dexamethasone (DEXA) (0.5 mg/kg/day) for the periods shown; indicated parameters were contrasted with control values. Voltages were obtained by cable and equivalent circuit analysis and evaluation of voltage divider ratios following impalement of single cells with microelectrodes. *Indicates significant difference (P <0.05) versus controls.

From Sansom and O'Neil 213
Figure 9. Figure 9.

Apical membrane partial ionic conductances (G) and currents (I) were determined for Na+ and K+ as a function of days of DOCA therapy (2 mg/kg/day). Cells impaled were presumed to be principal cells of rabbit cortical collecting tubule. *Indicates a significant difference (P <0.05) from day 0 values.

From Sansom and O'Neil 213
Figure 10. Figure 10.

Influence of in vitro aldosterone (ALDO) or dexamethasone (DEX) on bicarbonate reabsorption in isolated microperfused OMCDis from adrenalectomized rabbits. Steroids or diluent were added to the bath following a 90‐min preequilibration period. JHCO3 rates are shown for the pre‐ and poststeroid periods.

From Stone et al. 234
Figure 11. Figure 11.

Determinants of SNGFR in normal control hydropenic rats and in hydropenic rats treated with the glucocorticoid methylprednisolone for 4 days. In addition to SNGFR, the following parameters are shown: QA (glomerular plasma flow rate); ΔP (hydraulic pressure difference across the glomerular capillary wall); πA, πE (afferent and efferent arteriolar oncotic pressures; and RA, RE (afferent and efferent arteriolar resistances).

From Baylis and Brenner 15


Figure 1.

Aldosterone‐stimulated short‐circuit current (SCC) in toad bladder. Aldosterone (0.28 μM) or diluent was added to serosal surface of paired bladders obtained from toads soaked 3–5 days in either water or saline. Diminished response in toads soaked for long periods in saline as seen in this study has been noted by others 225.

from Crabbe 35


Figure 2.

Influence of amphotericin B on short‐circuit current (SCC) in toad bladder compared to that of vasopressin. When amphotericin B was added to apical membrane, a rapid rise in SCC occurred that was not augmented by subsequent addition of vasopressin (solid line). Amphotericin B addition after vasopressin, however, enhanced SCC beyond that seen with vasopressin alone.

From Lichenstein and Leaf 157


Figure 3.

Schematic of relative nuclear versus cytoplasmic labeling of [3H]aldosterone and [3H]SC 26304, a spirolactone. After the portal vein and hepatic artery were ligated, adrenalectomized rats were injected IV with either [3H]aldosterone or [3H]SC 26304 and the kidneys removed 2 or 10 min later. Nonspecific binding was determined in rats injected with [3H]steroid and a 100‐fold excess of unlabeled D‐aldosterone. Scale at left is in terms of mol × 10−14/mg protein. The results show that even though cytoplasmic labeling of mineralocorticoid receptors with [3H]SC 26304 exceeds that of [3H]aldosterone, only [3H]aldosterone‐receptor complexes are retained by nuclear chromatin. Furthermore, the absolute amount of [3H]aldosterone retained at 10 min exceeded that at 2 min, despite the fact that cytoplasmic labeling was significantly reduced because of the corresponding fall in plasma levels of [3H]steroid.

Adapted from Marver et al. 172


Figure 4.

Relative specific binding of three corticosteroids along the adrenalectomized rat or rabbit nephron. Binding activity was determined using either in vivo administration of [3H]dexamethasone and subsequent autoradiography of tissue segments, or in vitro binding assays with isolated segments and either [3H]aldosterone or [3H]corticosterone. Aldosterone and dexamethasone studies utilized rabbits; corticosterone studies, rats.

Adapted from the studies of Doucet and Katz 47, Farman et al. 69, Lee et al. 154


Figure 5.

Relationship between steady‐state plasma aldosterone concentration and flux of sodium and potassium in rabbit cortical collecting tubule. Closed circles represent the lumen‐to‐bath 22Na tracer flux; open circles represent net K+ transport determined on luminal samples monitoring perfused and collected K+ concentrations. There was no significant difference in bath‐to‐lumen tracer 22Na flux measured in several groups having both high and low plasma aldosterone levels. Overall average was 1.4 pEq/cm‐s, and group averages ranged from 1.0 to 1.7 pEq/cm‐s.

adapted from the study of Schwartz and Burg 216


Figure 6.

Influence of aldosterone on electrolyte handling by adrenalectomized rat: inhibition of the response by actinomycin D. Animals were adrenalectomized 24 h prior to the study and maintained on 0.035 M NaCl drinking water without food. They were given diluent (control) or aldosterone (1 μg/kg BW loading dose +1 μg/kg/h infusion) ± 300 μg/kg actinomycin D. Some controls received only actinomycin D. Shown at the top are plasma Na+ and K+ concentrations as a function of time following initiation of study. At the bottom is shown either fractional excretion of Na+ (FE Na) or urinary excretion of K+ (UKV).

From Horisberger and Diezi 118


Figure 7.

Influence of aldosterone on CCD Na+,K+‐ATPase activity. Upper panel: Na+,K+‐ATPase activities in mol/kg dry tubule wt/h at 37°C in CCDs obtained from normal (NORM) rabbits are denoted by the solid bar (±SEM). Stippled bars include activities seen in CCDs from adrenalectomized (ADX) rabbits injected at time 0 with diluent or 10 μg/kg BW aldosterone (ALDO) ± the spirolactone SC 26304 (SPIRO), or 100 μg‐kg BW dexamethasone (DEX) and sacrificed at either 1.5 or 3 h. Bottom panel: Na+,K+‐ATPase activities at 3 h postinjection of: (1) diluent (ADX); (2) 10 μg‐kg BW aldosterone (ALDO); or (3) 10μg/kg BW aldosterone + a total of 5 mg/kg BW amiloride (AMIL) given in four split doses, starting at t= −30 min.

Adapted from Petty et al. 195


Figure 8.

Influence of corticosteroid therapy on transepithelial voltage (Vte) and the voltage across the apical (Va) and basolateral (Vb) membrane of the cortical collecting tubule principal cell. Rabbits were treated with DOCA (2 mg/kg/day) or dexamethasone (DEXA) (0.5 mg/kg/day) for the periods shown; indicated parameters were contrasted with control values. Voltages were obtained by cable and equivalent circuit analysis and evaluation of voltage divider ratios following impalement of single cells with microelectrodes. *Indicates significant difference (P <0.05) versus controls.

From Sansom and O'Neil 213


Figure 9.

Apical membrane partial ionic conductances (G) and currents (I) were determined for Na+ and K+ as a function of days of DOCA therapy (2 mg/kg/day). Cells impaled were presumed to be principal cells of rabbit cortical collecting tubule. *Indicates a significant difference (P <0.05) from day 0 values.

From Sansom and O'Neil 213


Figure 10.

Influence of in vitro aldosterone (ALDO) or dexamethasone (DEX) on bicarbonate reabsorption in isolated microperfused OMCDis from adrenalectomized rabbits. Steroids or diluent were added to the bath following a 90‐min preequilibration period. JHCO3 rates are shown for the pre‐ and poststeroid periods.

From Stone et al. 234


Figure 11.

Determinants of SNGFR in normal control hydropenic rats and in hydropenic rats treated with the glucocorticoid methylprednisolone for 4 days. In addition to SNGFR, the following parameters are shown: QA (glomerular plasma flow rate); ΔP (hydraulic pressure difference across the glomerular capillary wall); πA, πE (afferent and efferent arteriolar oncotic pressures; and RA, RE (afferent and efferent arteriolar resistances).

From Baylis and Brenner 15
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Article Title: Corticosteroids and the Kidney
 

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Diana Marver. Corticosteroids and the Kidney. Compr Physiol 2011, Supplement 25: Handbook of Physiology, Renal Physiology: 1543-1576. First published in print 1992. doi: 10.1002/cphy.cp080232