Influence of enalapril on established pressure-overload cardiac hypertrophy in low and normal renin states in female rats

To determine whether effects of angiotensin converting enzyme (ACE) inhibit ors on well-established pressure overload-induced cardiac hypertrophy and c oronary remodeling depend upon normal plasma renin levels, the influence of enalapril on ventricular mass and coronary vascular resistance (CVR) was d etermined in a low-renin female rat model of chronic pressure overload,(deo xycorticosterone acetate hypertension, DOCA), and compared to its effect in a normal-renin model, (aortic constriction, AC). Six weeks after experimen t initiation, plasma renin activity of DOCA-treated rats was reduced to sim ilar to 12% that of sham-treated and AC-treated groups. Enalapril was then added to the drinking water of half the animals in each group for two addit ional weeks. Comparing experimental groups to controls, this delayed enalap ril treatment had 1) no effect on the elevated arterial pressures, 2) no ef fect on the elevated coronary resistance, and, in the DOCA group; 3) no eff ect on cardiac hypertrophy. However, this brief enalapril treatment reduced absolute and relative ventricular weights of AC rats. These data suggest t hat circulating renin is required for the anti-hypertrophic efficacy of lat e-onset brief treatment with enalapril. Since enalapril-induced reversal of cardiac hypertrophy in AC:AC rats was not accompanied by reversal of coron ary remodeling, growth signals other than angiotensin II may be involved in coronary remodeling.