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 enzy me (ACE) inhibition with captopril prevents the development of hyperte nsion and myocardial hypertrophy and affects nitric oxide synthase (NO S) activity in rats Animals were divided into five groups control two groups receiving N-G-nitro-L-arginine methyl ester (L-NAME) 20 or 40 m g/kg/day, a group receiving captopril 100 mg/kg/day and a group concom itantly treated with 40 mg/kg/day L-NAME pins 100 mg/kg/day captopril. After four weeks, systolic blood pressure (SEP) significantly increas ed in both L-NAME groups by 30 % and 34 %, respectively. In the captop ril group, SEP significantly decreased by 30 % and in the captopril pl us L-NAME group SEP was not changed as compared to the control Althoug h left ventricular weight/body weight (LVW/BW) ratio in both L-NAME gr oups was significantly elevated by 19 % and 29 %, respectively, no alt erations in LVW/BW ratio were found in the captopril group and captopr il plus L-NAME group. In both groups receiving L-NAME, NOS activity si gnificantly 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 th e kidney, respectively. Captopril did not influence NO synthase activi ty in any of the studied tissues. We conclude that captopril prevents the development of hypertension and LV hypertrophy without affecting N O formation.