Captopril prevents NO-deficient hypertension and left ventricular hypertrophy without affecting nitric oxide synthase activity in rats.

The aim of the study was to assess whether angiotensin converting enzyme (ACE) inhibition with captopril prevents the development of hypertension and myocardial hypertrophy and affects nitric oxide synthase (NOS) activity in rats. Animals were divided into five groups: control, two groups receiving NG-nitro-L-arginine methyl ester (L-NAME) 20 or 40 mg/kg/day, a group receiving captopril 100 mg/kg/day and a group concomitantly treated with 40 mg/kg/day L-NAME plus 100 mg/kg/day captopril. After four weeks, systolic blood pressure (SBP) significantly increased in both L-NAME groups by 30% and 34%, respectively. In the captopril group, SBP significantly decreased by 30% and in the captopril plus L-NAME group SBP was not changed as compared to the control. Although left ventricular weight/body weight (LVW/BW) ratio in both L-NAME groups was significantly elevated by 19% and 29%, respectively, no alterations in LVW/BW ratio were found in the captopril group and captopril plus L-NAME group. In both groups receiving L-NAME, NOS activity significantly decreased by 17% and 69% in the heart, by 14% and 26% in the aorta, by 60% and 73% in the brain and by 13% and 30% in the kidney, respectively. Captopril did not influence NO synthase activity in any of the studied tissues. We conclude that captopril prevents the development of hypertension and LV hypertrophy without affecting NO formation.