Role of angiotensin II in the hormonal, renal, and electrolyte response to sodium restriction.

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Abstract
Adrenal responses to angiotensin II (ANG II) are enhanced with restriction of sodium intake. To determine whether increased circulating ANG II levels are responsible for the enhanced responsiveness, the adrenal and blood pressure responses to ANG II in human subjects were assessed four times: in balance on a high and a low salt diet and before and after the administration of a converting enzyme inhibitor (enalapril). Before enalapril administration, sodium restriction significantly increased (p less than 0.02) plasma renin activity, ANG II, and aldosterone levels; the aldosterone response to ANG II was enhanced twofold (p less than 0.01); and the blood pressure response to ANG II infusion was reduced significantly (p less than 0.05). Despite a fixed and low plasma ANG II concentration when enalapril was employed, the adrenal response to ANG II on the low salt diet was enhanced to the same degree as that observed before administration of the converting enzyme inhibitor. Conversely, enalapril substantially altered the blood pressure response to ANG II with sodium restriction, completely preventing the reduction in responsiveness. If the subjects were first given enalapril and then sodium intake was restricted, ANG II levels did not change significantly but renal excretion of both sodium and potassium was substantially modified. The rate at which renal excretion of sodium fell to match intake was retarded strikingly (p less than 0.001); conversely, renal retention of potassium increased significantly (p less than 0.03) as low salt balance was attained. Possibly because of the potassium retention, aldosterone levels rose, but significantly less than when enalapril was absent.