What is normal aldosterone physiology?

Updated: Oct 19, 2018
  • Author: George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London); Chief Editor: Robert P Hoffman, MD  more...
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Aldosterone participates in the homeostasis of circulating blood volume and serum potassium concentration; these, in turn, feed back to regulate aldosterone secretion by the zona glomerulosa of the adrenal cortex. Aldosterone secretion is stimulated by an actual or apparent depletion in blood volume detected by stretch receptors and by an increase in serum potassium ion concentrations; it is suppressed by hypervolemia and hypokalemia.

The mechanisms regulating aldosterone secretion are complex, involving the zona glomerulosa of the adrenal glands, the juxtaglomerular apparatus in the kidneys, the cardiovascular system, the autonomic nervous system, the lungs, and the liver (see the image below). The major factors stimulating aldosterone production and release by the zona glomerulosa are angiotensin II and the serum potassium concentration. The juxtaglomerular apparatus is the principal site of regulation of angiotensin II production.

Physiologic regulation of the renin-angiotensin-al Physiologic regulation of the renin-angiotensin-aldosterone axis.

ACTH stimulates aldosterone secretion in an acute and transient fashion but does not appear to play a significant role in the long-term regulation of mineralocorticoid secretion. The major inhibitors of the zona glomerulosa include circulating atrial natriuretic peptide (ANP) and, locally, dopamine. Although ANP levels are clearly increased in hyperaldosteronism, neither ANP nor dopamine has been implicated as a primary cause of clinically disordered aldosterone secretion.

Metoclopramide has been shown to increase aldosterone secretion, suggesting that dopamine may tonically inhibit aldosterone release. The physiologic roles of adrenomedullin and vasoactive intestinal peptide (VIP) on aldosterone secretion remain to be clarified, although both of these neuropeptides are produced in rat zona glomerulosa.

The synthesis of prorenin, its conversion to renin, and its systemic secretion are stimulated by blood volume contraction detected by stretch receptors, beta-adrenergic stimulation of the sympathetic nervous system, and prostaglandins I2 and E2. These processes are inhibited by volume expansion and ANP.

Renin converts angiotensinogen, a proenzyme synthesized in the liver, into the decapeptide angiotensin I, which is then converted in the lungs into the octapeptide angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is both a stimulator of aldosterone secretion and a potent vasopressor. Angiotensin II is metabolized to angiotensin III, a heptapeptide that is also a stimulator of aldosterone secretion.

The synthesis and secretion of prostaglandins I2 and E2 and the normal function of the stretch receptors are dependent on the intracellular ionized calcium concentration. Renal prostaglandin secretion is stimulated by catecholamines and angiotensin II. The complex regulation of aldosterone synthesis and secretion provides several points at which disturbance in the regulation of aldosterone secretion may occur.

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