Effect of captopril in L-name-induced hypertension on the rat myocardium, aorta, brain and kidney

Long-term administration of NC-nitro-L-arginine methyl ester (L-NAME) induc es development of hypertension and hypertrophy of the left ventricle in rat s. The aim of the present study was to demonstrate the effect of chronic L- NAME treatment on DNA and RNA concentration, and protein synthesis in the r at heart, aorta, brain and kidney and to determine the effect of angiotensi n converting enzyme (ACE) inhibitor captopril on these potential alteration s. Four groups of rats were investigated: control, L-NAME (40 mg kg(-1) day (-1)), captopril (100 mg kg(-1) day(-1)), and L-NAME (40 mg kg(-1) day(-1)) + captopril (100 mg kg(-1) day(-1)). NO synthase activity in the heart, ao rta, brain and kidney was found to be decreased in the L-NAME group. In the group of rats treated with L-NAME + captopril, captopril did not affect NO synthase inhibition. Captopril, however, completely prevented development of hypertension and left Ventricular hypertrophy in this group. In the L-NA ME group, DNA and RNA concentrations, as well as [C-14]leucine incorporatio n, were significantly increased in all the tissues investigated. In the L-N AME + captopril group, captopril completely prevented the enhancement of DN A and RNA concentrations and [C-14]leucine incorporation in all tissues com pared to the L-NAME group. Moreover, a significant decrease in RNA concentr ation and [C-14]leucine incorporation below control values was found in the captopril group as well as the L-NAME + captopril group in all the tissues investigated. We conclude that captopril prevented the development of hype rtension and increase in nucleic acid concentration and protein synthesis i n the heart, aorta, brain and kidney in rats treated with L-NAME + captopri l. However, this protective effect of captopril was not associated with inc reased NO synthase activity in this model of hypertension.