Control of aldosterone secretion during sodium restriction: Adrenal receptor regulation and increased adrenal sensitivity to angiotensin II

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Abstract
The mechanism of increased adrenal sensitivity to angiotensin II during the aldosterone response to Na restriction was investigated in the rat. Na restriction for 36 h increased the aldosterone-stimulating effect of low-dose (1 ng/min) infusion of angiotensin II [A II] and enhanced binding of 125I-labeled A II to the zona glomerulosa in vivo. In vivo binding of 125I-labeled angiotensin II significantly decreased after 36 h of high-Na intake. In isolated glomerulosa cells, increased A II binding after Na restriction apparently resulted from a significant increase in receptor affinity (+80%) and a smaller increase in receptor concentration (+25%). The corresponding aldosterone responses in dispersed cells showed an increase in A II sensitivity, commensurate with increased receptor affinity. More prolonged Na restriction (4 days) caused a further increase in angiotensin receptor concentration (+70%) and maximal aldosterone response (+50%); binding affinity of adrenal receptors and sensitivity of the in vitro aldosterone response had returned to normal. During Na loading for 36 h and 4 days, the converse effects on adrenal A II receptors and aldosterone production were observed. In contrast to the consistent increase in A II receptors in adrenal glands of Na restricted animals, A II binding capactiy of uterine smooth muscle was decreased by 40% after 7 days of Na restriction. Rapid regulation of receptor affinity and concentration during changes in Na intake provided a basis for dynamic modulation of aldosterone responses by dietary Na content. During Na restriction, sequential changes in receptor affinity and concentration account for enhanced binding and steroidogenic actions of A II in vivo and in vitro. These receptor changes and converse effects of Na loading may serve as a local regulatory mechanism in physiological control of adrenal sensitivity and aldosterone secretion. The opposite finding in smooth muscle-that Na restriction decreased A II concentration receptors-is consistent with divergent effects of changing Na balance upon vascular and adrenal responses to A II.