Effect of inhibition of angiotensin II with captopril on renal overflow of norepinephrine.

Abstract

To determine whether endogenously generated angiotensin II (AII) enhances the release of norepinephrine from sympathetic axon terminals in the kidney, the concentration of norepinephrine in renal vein plasma was determined in the dog during renal stimulation (12 V, 3 ms, 5 Hz, for 15 min) under control conditions and after administration of the angiotensin converting-enzyme inhibitor, captopril. Captopril was administered at a dose that completely inhibited the mean arterial pressure and renal blood flow effects of 0.2 .mu.g/kg of angiotensin I (AI). During control conditions (n = 13), nerve stimulation increased the rate of renal renin secretion (P < 0.01) and, therefore, the generation of AII. Under both control conditions and after captopril administration (n = 12), renal nerve stimulation decreased renal blood flow (P < 0.001) and increased renal vascular resistance (P < 0.001) and the renal venous concentration of prostaglandin E2 (P < 0.05). There were no significant differences in the magnitude of these effects between the 2 groups of dogs. Similarly, the concentration of norepinephrine in renal venous plasma was increased by nerve stimulation in both control dogs and captopril-treated dogs (P < 0.001), and there was no difference in the magnitude of this effect. The renal hemodynamic and renal venous norepinephrine responses evoked by direct renal nerve stimulation were not influenced by the blockade of the converting enzyme with captopril. Endogenously generated AII does not facilitate the release of norepinephrine from axon terminals in the canine kidney. The acute administration of captopril does not interfere with postganglionic sympathetic nerve function. [During hypotensive hemorrhage, intrarenal AII is several times higher than plasma AII.].