Captopril-induced hyperreninemia in cholesterol-fed rabbits.

The aims of this study were to investigate the potential effects of captopril (CPT)-induced chronic hyperreninemia on atherogenesis, and to describe and quantitate the morphological changes which occur in the juxtaglomerular (JG) apparatus of drug-treated rabbits. Four groups of normotensive New Zealand rabbits were used. Drug control groups were fed regular rabbit chow (Group I), or regular chow supplemented with cholesterol (Group III). Group II animals were fed regular chow and treated with captopril, and Group IV animals were fed the cholesterol-diet and treated with captopril. Daily captopril administration for a period of six months resulted in significantly (p less than 0.001) increased levels of plasma renin activity and blood urea nitrogen. Mean systemic arterial pressure, plasma aldosterone levels, and hematocrits were significantly reduced in the CPT-treated animals as compared to untreated control groups. No effect on atherogenesis was found. Morphometric analysis showed no difference in the size of the glomeruli between the untreated and the CPT-treated, normal-diet groups, however, significant (p less than 0.001) hypertrophy and hyperplasia of the JG complex were observed in all CPT-treated animals. It is concluded that captopril-induced reductions in systemic arterial blood pressure and perfusion pressure, in concert with a blocked renin-angiotensin system which interferes with the normal autoregulation of renal blood flow and glomerular filtration, leads to significant morphologic and functional alterations in the kidney of normotensive animals.