Renal, adrenal and vascular changes during inhibition of converting enzyme with captopril.

Abstract

1. In rats treated continuously with captopril (80 microgram/h, i.p.), for 2 days, blood pressure decreased and adrenal angiotensin II receptor concentration was decreased from 160 fmol/mg protein (s.e.m. = 9) in controls to 131 fmol/mg protein (s.e.m. 7, P < 0.01, n = 10). However, after 5 days of continuous treatment, blood pressure had returned to normal and adrenal receptor concentrations in treated rats were not significantly different from controls (180 fnol/mg, s.e.m. = 11 and 203 fmol/mg protein s.e.m. = 14 respectively, 0.1 > P > 0.05). 2. Vascular reactivity, defined as the pressor response to exogenous angiotensin II, increased concurrently by 166 and 33% respectively. 3. In anaesthetized dogs (n = 8), captopril (1.5 mg/kg, i.v.) caused a fall in blood pressure, and uring bradykinin excretion increased from 1-08 (s.e.m. = 0.14) to 1.64 microgram/h (s.e.m. = 0.33, P < 0.025) at 15 min. Renal blood flow increased significantly (P < 0.01) with no change in glomerular filtration rate, and there was no change in either renal venous or arterial blood bradykinin levels. 4. Thus, converting enzyme inhibition produces transient secondary changes in angiotensin receptors and vascular reactivity. Increased urine bradykinin probably reflects decreased catabolism of intrarenal bradykinin. The hypotensive effect of captopril may be due in part to raised levels of bradykinin in the kidney.