The synthesis and secretion of the principal mineralocorticoid aldosterone in the adrenal zona glomerulosa are stimulated by potassium ions, ACTH, serotonin, and b-endorphins, and are inhibited by dopamine, somatostatin, and atrial natriuretic peptide. However, the primary regulatory system of aldosterone is the renin-angiotensin system. Renin release from the kidney juxtaglomerular apparatus is stimulated by the integrated effects of a number of mechanisms, including a decrease in renal blood flow (through volume-sensitive stretch receptors in the renal afferent arterioles), b-adrenergic activity, and a low sodium concentration of the tubular fluid sensed by the macula densa. Renin converts angiotensinogen to angiotensin I, which in turn is cleaved by the angiotensin-converting enzyme to form angiotensin II which is a strong vasoconstrictor and stimulator of aldosterone secretion. Aldosterone is much less under the control of ACTH than cortisol. The principle actions of aldosterone are promotion of sodium reabsorption linked to excretion of potassium, and to a lesser extent hydrogen ions, in the distal renal tubules and collecting ducts. Aldosterone also affects sodium excretion via the gut and the salivary and sweat glands.

Failure to produce aldosterone results in renal sodium wasting with concomitant water loss and potassium retention. Partial compensation occurs with stimulation of the renin-angiotensin system and ADH secretion.

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