Intrarenal role of angiotensin II and [des-Asp1]angiotensin II

Abstract

The relative importance of angiotensin II (AII) and its heptapeptide fragment [des-Asp1]AII (AIII) in regulating renal hemodynamics and electrolyte excretion was investigated in anesthetized dogs. Intrarenal infusion of the heptapeptide antagonist [des-Asp1,Ile8]AII for 90 min in 7 Na-depleted dogs caused no significant changes in renal hemodynamics, electrolyte excretion or arterial pressure. Renal arterial infusion of the converting enzyme inhibitor SQ 20881 caused marked increases in renal blood flow (RBF) (32%), and urinary Na excretion (450%), K (56%) and H2O (60%), small increases in glomerular filtration rate (GFR) (11%), and no significant changes in plasma aldosterone concentration. When renal artery pressure (RAP) was reduced, RBF and GFR were effectively autoregulated in normal and Na-depleted control dogs and in dogs infused with AIII antagonist. In normal and Na-depleted dogs infused with SQ 20881, RBF was effectively autoregulated, but GFR, filtration fraction and calculated efferent arteriolar resistance decreased progressively as RAP was reduced. The renin-angiotensin system has an important intrarenal role in controlling electrolyte excretion and in autoregulation of GFR, probably via an efferent arteriolar mechanism. AIII, compared to AII, plays a relatively minor role in the renal response to Na depletion and reduced RAP.