Atrial natriuretic factor, angiotensin II, and the slow component of renal autoregulation

Publisher Website
Google Scholar
Abstract
Autoregulation of renal blood flow is highly efficient and is mediated partly by tubuloglomerular feedback (TGF), which couples regulation of blood flow to that of sodium excretion. Atrial natriuretic factor (ANF) dilates preglomerular resistance vessels, in which autoregulation occurs, and has been reported to inhibit TGF. This study addressed potential actions of ANF on the slow, TGF-mediated, component of autoregulation. Renal blood flow was measured by an electromagnetic flow probe in Sprague – Dawley rats anesthetized by halothane or isoflurane while renal perfusion pressure was manipulated by a servo-controlled clamp placed on the aorta between the renal arteries. Progressive reduction of perfusion pressure to 60 mmHg (1 mmHg = 133.3 Pa) induced resetting of autoregulation to operate at the reduced pressure and to defend lower renal blood flow. Infusion of ANF at a dose shown to reliably increase sodium excretion did not affect autoregulation or its resetting. Because resetting is angiotensin II dependent, the converting enzyme inhibitor Enalaprilat® was used to provide angiotensin II blockade. As expected, autoregulation did not reset to operate at reduced perfusion pressure. Again ANF was without effect. In a third experiment, relaxation of resistance was assessed in response to repeated steps of perfusion pressure between 65 and 75 mmHg. Time constants of constriction and dilatation were recovered by fitting to a single exponential before and during ANF infusion. Time constants ranged from 0.045 to 0.055 Hz, were consistent with operation of TGF, were not different for constriction or dilatation, and were unaltered by ANF; nor did ANF affect the magnitude of constriction or dilatation. Autoregulation compensated for ≈ 87% of the increase and ≈ 79% of the decrease in driving pressure during control. During ANF infusion it compensated for ≈ 98% of the increase and ≈ 82% of the decrease. The results indicate that, although ANF and angiotensin II act on the same resistance vessels, ANF does not attenuate angiotensin II dependent resetting of renal autoregulation; nor does ANF inhibit the slow component of renal autoregulation.Key words: resistance, tubuloglomerular feedback, time constant.

This publication has 0 references indexed in Scilit: