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Aldosterone

Arunabha Ganguly

10.1002/cphy.cp070305

Source: Supplement 22: Handbook of Physiology, The Endocrine System, Endocrine Regulation of Water and Electrolyte Balance

Originally published: 2000

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Regulation of Synthesis and Secretion
1.1 Agents Stimulating Aldosterone Secretion
1.2 Agents Inhibiting Aldosterone Secretion
1.3 Other Factors
1.4 Pathophysiological Regulation of Aldosterone Secretion
2 Cellular Actions
2.1 Receptors
2.2 11β‐Hydroxysteroid Dehydrogenase
2.3 Sodium Channel
2.4 Sodium‐Potassium Adenosinetriphosphatase
2.5 Effects on the Kidney
2.6 Effects on the Colon
2.7 Effects on the Vascular Smooth Muscle
2.8 Effects on the Brain
2.9 Effects on the Skin
2.10 Effects on the Heart
2.11 Possible Non‐genomic Effects
Figure 1. Figure 1.

Regression lines of plasma adosterone and plasma angiotensin II (AII) levels during AII infusion on a low‐ (open circles) or high‐ (closed circles) sodium diet in normal humans. [From Hollenberg et al. 294.]
Figure 2. Figure 2.

Slopes of the plasma aldosterone responses to angiotensin II infusion in sodium‐deplete (open circles) or ‐replete (closed circles) states in normal humans. [From Oelkers et al. 495.]
Figure 3. Figure 3.

Effects of addition of nitrendipine during different time points of incubation (5 min, left, and 30 min, right) of bovine adrenal glomerulosa cells on angiotensin II‐ and K+‐induced aldosterone secretion. [From Ganguly et al. 230.]
Figure 4. Figure 4.

Concentration‐dependent changes in cytosolic free calcium concentration in response to angiotensin II (ANGII) in cultured bovine adrenal glomerulosa cells. [From Kramer 370.]
Figure 5. Figure 5.

Inhibitory effect of calmidazolium, a calmodulin inhibitor on angiotensin II‐ and K+‐induced aldosterone secretion from bovine adrenal glomerulosa cells. [From Ganguly et al. 230.]
Figure 6. Figure 6.

Slopes of plasma aldosterone responses to K+ infusion on a high‐ or low‐sodium or ‐K+ diet. [From Dluhy et al. 161.]
Figure 7. Figure 7.

Interactive effects, in a three‐dimensional mode, of plasma K+ and aldosterone on renal K+ excretion. [From Young 738.]
Figure 8. Figure 8.

Effects of K+ and angiotensin II (AII; shows by digital imaging and microfluorometry) on single rat adrenal glomerulosa cells. B: Control fluoroscent image of cell. C, D, and E: Changes in cell Ca2+ after K+ increase in the medium at 0.5 and 1.5 min after K+ increase, then at 4 min upon reintroduction of basal K+level in the medium. F, G, and H: Same protocol with AII. [From Connor et al. 139.]
Figure 9. Figure 9.

Effects of K+ and angiotensin II on inositol trisphosphate (IP3 formation and aldosterone production in bovine adrenal glomerulosa cells. [From Ganguly et al. 229.]
Figure 10. Figure 10.

Rat adrenal glomerulosa (G) and fasciculata (F/reticularis (R) zones at low power (left) and high power (right) as stained by specific antibody to aldosterone synthase in sodium‐replete (upper panel) and sodium‐deplete (lower panel) states. M = medulla. [From Ogishima et al. 500.]
Figure 11. Figure 11.

Changes in angiotensin II receptors in rat adrenal glomerulosa cells in control (open squares), sodium‐restricted (open circles), and sodium‐restricted rats treated with a converting enzyme inhibitor (closed circles). [From Aguilera et al. 14.]
Figure 12. Figure 12.

Potentiation of corticotropin‐stimulated aldosterone secretion by endothelin‐1. Open triangles, control; open circles, endothelin infusion; closed circles, corticotropin (250 μg intravenous infusion); and closed triangles, corticotropin + endothelin infusion. [From Vierhapper et al. 683.]
Figure 13. Figure 13.

Effects of atrial natriuretic peptide (ANP) on angiotensin II (AII)‐mediated aldosterone secretion in bovine adrenal glomerulosa cells. Closed circles, AII; closed squares AII + ANP; closed triangles, AII + 8‐bromo cyclic guanosine monophosphate. [From Ganguly et al. 232.]
Figure 14. Figure 14.

No effects of atrial natriuretic peptide (ANP) or cyclic guanosine monophosphate (cGMP) seen on inositol trisphosphate formation in bovine adrenal glomerulosa cells. Closed circles, angiotensin II (AII), closed squares, AII + ANP; closed triangles, AII + 8‐bromo cGMP. [From Ganguly et al. 232.]
Figure 15. Figure 15.

Metoclopramide‐induced changes in plasma aldosterone and prolactin levels with (open circles) or without (closed circles) dopamine infusion. [From Carey et al. 109.]
Figure 16. Figure 16.

Receptors of the steroid and other members of the superfamily along with mineralocorticoid receptor (MR) structure scheme. The solid black area represents the DNA‐binding domain and the hatched area, the ligand binding region. PR, progesterone receptor; AR, androgen receptor; GR, glucocorticoid receptor; ER, estrogen receptor; T3 R, triiodothyronine receptor; RAR, retinoic acid receptor; VDR, vitamin D receptor. [From Funder 216.]
Figure 17. Figure 17.

Mineralocorticoid receptor (MR) in rabbit renal cortex, by immunocytochemistry using a specific antiidiotypic MR antibody. A: Distal and connecting tubules. B: Cortical collecting tubule under higher magnification. [From Farman 199.]
Figure 18. Figure 18.

Nuclear surface of aldosterone‐sensitive Madin‐Darby canine kidney cell by atomic force microscopy. a: Apical nuclear surface. b: Patch of nuclear surface; nuclear pores can be seen. c: Nuclear surface showing pores as light areas. d: Individual nuclear pore with a channel. [From Oberleithner et al. 493.]
Figure 19. Figure 19.

Renal tissue stained with a specific antibody directed at type 2 II β‐hydroxysteroid dehydrogenase. A: Cortex, thick ascending loop of Henle and distal tubule. B: Medulla. C: Papilla. D: Glomerulosa. [From Smith 631.]
Figure 20. Figure 20.

Expression of three subunits (α, β, and γ) of sodium channels in the kidney (a–c) and salivary glands (d–f). Bright‐field and dark‐field photographs. [From Duc et al. 172.]
Figure 21. Figure 21.

Effects of aldosterone or spironolactone on the mRNAs (A) and immunoprecipitated proteins (B) of Na‐K‐ATPase subunits as well as sodium transport (C), measured by changes in electrical current and voltage in A6 cells. [From Verrey 680.]
Figure 22. Figure 22.

Rabbit renal collecting tubules: principal cells (PC) and intercalated cells (IC), a: Control rabbit tubule. b: Deoxycorticosterone acetate‐treated rabbit tubule. c: Dexamethasone‐treated rabbit tubule. [From Wade et al. 690.]
Figure 23. Figure 23.

Model of cellular transport of sodium and K+ through the apical and basolateral membranes of the principal cell (PC) of the cortical collecting duct. IC, intercalated cell. [From O'Neil 509.]
Figure 24. Figure 24.

Model of aldosterone action in rabbit cortical collecting duct principal cell. A: Control cell. B: Aldosterone effect. Effects of aldosterone on sodium and K+ channels and Na‐K‐ATPase are shown schematically. [From O'Neil 509.]


Figure 1.

Regression lines of plasma adosterone and plasma angiotensin II (AII) levels during AII infusion on a low‐ (open circles) or high‐ (closed circles) sodium diet in normal humans. [From Hollenberg et al. 294.]



Figure 2.

Slopes of the plasma aldosterone responses to angiotensin II infusion in sodium‐deplete (open circles) or ‐replete (closed circles) states in normal humans. [From Oelkers et al. 495.]



Figure 3.

Effects of addition of nitrendipine during different time points of incubation (5 min, left, and 30 min, right) of bovine adrenal glomerulosa cells on angiotensin II‐ and K+‐induced aldosterone secretion. [From Ganguly et al. 230.]



Figure 4.

Concentration‐dependent changes in cytosolic free calcium concentration in response to angiotensin II (ANGII) in cultured bovine adrenal glomerulosa cells. [From Kramer 370.]



Figure 5.

Inhibitory effect of calmidazolium, a calmodulin inhibitor on angiotensin II‐ and K+‐induced aldosterone secretion from bovine adrenal glomerulosa cells. [From Ganguly et al. 230.]



Figure 6.

Slopes of plasma aldosterone responses to K+ infusion on a high‐ or low‐sodium or ‐K+ diet. [From Dluhy et al. 161.]



Figure 7.

Interactive effects, in a three‐dimensional mode, of plasma K+ and aldosterone on renal K+ excretion. [From Young 738.]



Figure 8.

Effects of K+ and angiotensin II (AII; shows by digital imaging and microfluorometry) on single rat adrenal glomerulosa cells. B: Control fluoroscent image of cell. C, D, and E: Changes in cell Ca2+ after K+ increase in the medium at 0.5 and 1.5 min after K+ increase, then at 4 min upon reintroduction of basal K+level in the medium. F, G, and H: Same protocol with AII. [From Connor et al. 139.]



Figure 9.

Effects of K+ and angiotensin II on inositol trisphosphate (IP3 formation and aldosterone production in bovine adrenal glomerulosa cells. [From Ganguly et al. 229.]



Figure 10.

Rat adrenal glomerulosa (G) and fasciculata (F/reticularis (R) zones at low power (left) and high power (right) as stained by specific antibody to aldosterone synthase in sodium‐replete (upper panel) and sodium‐deplete (lower panel) states. M = medulla. [From Ogishima et al. 500.]



Figure 11.

Changes in angiotensin II receptors in rat adrenal glomerulosa cells in control (open squares), sodium‐restricted (open circles), and sodium‐restricted rats treated with a converting enzyme inhibitor (closed circles). [From Aguilera et al. 14.]



Figure 12.

Potentiation of corticotropin‐stimulated aldosterone secretion by endothelin‐1. Open triangles, control; open circles, endothelin infusion; closed circles, corticotropin (250 μg intravenous infusion); and closed triangles, corticotropin + endothelin infusion. [From Vierhapper et al. 683.]



Figure 13.

Effects of atrial natriuretic peptide (ANP) on angiotensin II (AII)‐mediated aldosterone secretion in bovine adrenal glomerulosa cells. Closed circles, AII; closed squares AII + ANP; closed triangles, AII + 8‐bromo cyclic guanosine monophosphate. [From Ganguly et al. 232.]



Figure 14.

No effects of atrial natriuretic peptide (ANP) or cyclic guanosine monophosphate (cGMP) seen on inositol trisphosphate formation in bovine adrenal glomerulosa cells. Closed circles, angiotensin II (AII), closed squares, AII + ANP; closed triangles, AII + 8‐bromo cGMP. [From Ganguly et al. 232.]



Figure 15.

Metoclopramide‐induced changes in plasma aldosterone and prolactin levels with (open circles) or without (closed circles) dopamine infusion. [From Carey et al. 109.]



Figure 16.

Receptors of the steroid and other members of the superfamily along with mineralocorticoid receptor (MR) structure scheme. The solid black area represents the DNA‐binding domain and the hatched area, the ligand binding region. PR, progesterone receptor; AR, androgen receptor; GR, glucocorticoid receptor; ER, estrogen receptor; T3 R, triiodothyronine receptor; RAR, retinoic acid receptor; VDR, vitamin D receptor. [From Funder 216.]



Figure 17.

Mineralocorticoid receptor (MR) in rabbit renal cortex, by immunocytochemistry using a specific antiidiotypic MR antibody. A: Distal and connecting tubules. B: Cortical collecting tubule under higher magnification. [From Farman 199.]



Figure 18.

Nuclear surface of aldosterone‐sensitive Madin‐Darby canine kidney cell by atomic force microscopy. a: Apical nuclear surface. b: Patch of nuclear surface; nuclear pores can be seen. c: Nuclear surface showing pores as light areas. d: Individual nuclear pore with a channel. [From Oberleithner et al. 493.]



Figure 19.

Renal tissue stained with a specific antibody directed at type 2 II β‐hydroxysteroid dehydrogenase. A: Cortex, thick ascending loop of Henle and distal tubule. B: Medulla. C: Papilla. D: Glomerulosa. [From Smith 631.]



Figure 20.

Expression of three subunits (α, β, and γ) of sodium channels in the kidney (a–c) and salivary glands (d–f). Bright‐field and dark‐field photographs. [From Duc et al. 172.]



Figure 21.

Effects of aldosterone or spironolactone on the mRNAs (A) and immunoprecipitated proteins (B) of Na‐K‐ATPase subunits as well as sodium transport (C), measured by changes in electrical current and voltage in A6 cells. [From Verrey 680.]



Figure 22.

Rabbit renal collecting tubules: principal cells (PC) and intercalated cells (IC), a: Control rabbit tubule. b: Deoxycorticosterone acetate‐treated rabbit tubule. c: Dexamethasone‐treated rabbit tubule. [From Wade et al. 690.]



Figure 23.

Model of cellular transport of sodium and K+ through the apical and basolateral membranes of the principal cell (PC) of the cortical collecting duct. IC, intercalated cell. [From O'Neil 509.]



Figure 24.

Model of aldosterone action in rabbit cortical collecting duct principal cell. A: Control cell. B: Aldosterone effect. Effects of aldosterone on sodium and K+ channels and Na‐K‐ATPase are shown schematically. [From O'Neil 509.]

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Article Title: Aldosterone
 

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Arunabha Ganguly. Aldosterone. Compr Physiol 2011, Supplement 22: Handbook of Physiology, The Endocrine System, Endocrine Regulation of Water and Electrolyte Balance: 156-227. First published in print 2000. doi: 10.1002/cphy.cp070305