The three principal stimuli that increase aldosterone secretion are ACTH, angiotensin II, and hyperkalemia,
(i) ACTH stimulates the output of both aldosterone and deoxycortisone. However, the effect on aldosterone is transient – lasting a day or two – because a rise in aldosterone produces hypervolemia (which inhibits angiotensin-II production) and hypokalemia. Both these factors tend to lower aldosterone secretion.
In other words, in the presence of stronger controllers of aldosterone secretion (angiotensin-II, hyperkalemia), ATCH does not act as an important controller of aldosterone.
Thus, after hypophysectomy, the basal rate of aldosterone secretion is not immediately affected. However, chronic ACTH deficiency results in atrophy of the zona glomerulosa and leads to hypoaldosteronism.
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(ii) Angiotensin-II stimulates secretion of aldosterone. Angiotensin-II has an early action on the conversion of cholesterol to pregnenolone, and a late action on the conversion of corticosterone to aldosterone.
(iii) Hyper-kalemia is the most potent stimulator of aldosterone secretion. Like angiotensin II, K+ also stimulates the conversion of cholesterol to pregnenolone and the conversion of corticosterone to aldosterone.
Other factors affecting aldosterone secretion are as follows:
(i) Plasma Na+ concentration. A sharp fall in plasma Na+ of about 20 mEq/L stimulates aldosterone secretion, but such changes are rare,
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(ii) Posture. Plasma aldosterone concentration increases on prolonged standing. This increase is due to a decrease in the rate of removal of aldosterone from the circulation by the liver and an increase in aldosterone secretion due to a postural increase in renin secretion,
(iii) Diurnal variations, There is a circadian rhythm of aldosterone and renin secretion, with the highest values in the early morning before awakening,
(iv) Atrial natriuretic peptide (ANP). It inhibits renin secretion and decreases the responsiveness of the zona glomerulosa to angiotensin II.