Effects of captopril on salt appetite in sodium-replete rats and rats treated with desoxycorticosterone acetate (DOCA).

Abstract

Captopril (30 mg/kg daily by gavage), an orally active inhibitor of angiotensin-converting enzyme, reduced the intake of 0.15 M NaCl in rats treated with desoxycorticosterone acetate (2.5 mg/day S.C.). However, this is probably not a specific effect on salt appetite as captopril (30 or 60 mg/kg daily) did not reduce the intake of less palatable 0.5 M NaCl in desoxycorticosterone acetate-treated rats (1 or 2.5 mg daily). In contrast, captopril given alone (30 or 60 mg/kg daily) consistently caused a 3- to 5-fold increase in intake of 0.5 M NaCl that usually began on the 1st day and persisted until treatment stopped (1-3 weeks). Sodium intake and sodium excretion increased concomitantly, but the stimulation of salt appetite occurred even in the absence of sodium depletion. Also, the effect on salt appetite was specific; captopril did not increase the intake of 0.5 M KCl or 0.03 M sucrose. This potent and specific stimulation of sodium intake by oral treatment with an inhibitor of the renin-angiotensin system may be caused by a paradoxical increase in the synthesis of angiotensin II in the brain.