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  • Title: Regulation of aldosterone secretion: current concepts and newer aspects.
    Author: Bravo EL.
    Journal: Adv Nephrol Necker Hosp; 1977; 7():105-20. PubMed ID: 208405.
    Abstract:
    Four humoral factors have been shown to play important roles in the regulation of aldosterone secretion. These are ACTH, potassium, sodium and angiotensin II. ACTH appears to play little or no role in the maintenance of adrenal zona glomerulosa cells in response to specific stimuli. However, there is evidence to show that physiologic levels of ACTH regulate the minute-to-minute fluctuations of plasma aldosterone. In man and in experimental animals, alterations in potassium balance as well as acute increments in serum potassium can stimulate aldosterone production. The importance of potassium ion in the control of aldosterone secretion can be fully appreciated by the demonstration that aldosterone responses to other stimuli are subnormal in the presence of potassium depletion. Changes in dietary sodium can alter the aldosterone response to a number of acute stimuli. Sodium deprivation enhances aldosterone responses to ACTH infusion, potassium loading and angiotensin II administration. Enhanced conversion of corticosterone to aldosterone (due to sodium depletion) coupled with an acute stimulus acting at an earlier step in aldosterone biosynthesis probably explains the sensitizing effect of dietary sodium restriction. In recent years, indirect evidence has emerged to suggest that the COOH-terminal heptapeptide fragment of angiotensin II may mediate the aldosterone-stimulating activity of the renin-angiotensin system. The evidence has been derived from in vivo and in vitro studies indicating that angiotensin II and the heptapeptide stimulate aldosterone production equally well and that their relative binding potencies to adrenal zona glomerulosa cells are identical. In addition, heptapeptide antagonists are potent and specific inhibitors of angiotensin II-induced aldosterone biosynthesis. However, the data do not preclude the possibility that angiotensin II could stimulate aldosterone production without prior conversion to the heptapeptide.
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