Regulation of aldosterone secretion by the renin-angiotensin system during sodium restriction in rats.

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Abstract
The role of angiotensin II as mediator of the aldosterone response to short periods of Na restriction was studied in rats by administration of a converting enzyme inhibitor to block formation of the octapeptide throughout the duration of decreased Na intake. In control animals, short-term Na restriction caused increased levels of adrenal receptors for angiotensin II, with enhancement of early and late steps in aldosterone biosynthesis and elevation of plasma aldosterone concentration. Each of these changes induced by Na deficiency was abolished during blockade of angiotensin II formation by continuous infusion of the converting enzyme inhibitor, SQ 14,225 captopril. The absolute dependence of adrenal glomerulosa cell responses on angiotensin II formation indicated that the renin-angiotensin system is the primary regulator of aldosterone secretion during physiological fluctuations in Na intake.