Renal responses to atriopeptin II are not dependent on renal nerves
- 1 July 1986
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Vol. 251 (1) , R187-R191
- https://doi.org/10.1152/ajpregu.1986.251.1.r187
Abstract
The possibility that renal responses to atriopeptin II (AP II) may depend in part on an inhibition of renal sympathetic nerve effects on the kidney was investigated in seven anesthetized Wistar rats in which one of the kidneys was denervated 7-10 days before experimentation. Clearance studies were done before, during, and after infusion of AP II (0.07 nmol .cntdot. min-1 iv). During AP II infusion mean arterial pressure (MAP) decreased from 123 .+-. 2 to 75 .+-. 2 mmHg. Renal blood flow (RBF) was decreased significantly and renal vascular resistance was increased significantly in the innervated kidneys but not in the denervated kidneys during AP II infusion. Glomerular filtration rate during AP II infusion was not significantly altered, but urine flow rate and the excretion of sodium and potassium were significantly increased proportionately in both the innervated and denervated kidneys. These results suggest that 1) the decreased RBF observed in the innervated kidneys was due to an increase in renal vasoconstrictor nerve activity reflexly induced by the decrease in MAP during AP II infusion and 2) renal innervation was not necessary for AP II to produce a natriuresis and diuresis.This publication has 1 reference indexed in Scilit:
- Atrial extracts increase glomerular filtration rate in vivoAmerican Journal of Physiology-Renal Physiology, 1985