The mechanism by which intracerebroventricular administration of angiotensin II (AII) enhances renal sodium excretion was studied in anesthetized dogs. Intraventricular infusion of AII (6 ng/min) increased sodium excretion independently of changes in renal plasma flow (RPF), glomerular filtration rate (GFR), blood pressure (BP), and plasma concentration of aldosterone. In order to evaluate the intracerebral role of endogenous AII in the control of sodium excretion, the converting enzyme inhibitor, SQ20881 (0.5 μg/min), was infused intraventricularly in another group of dogs. This infusion decreased sodium excretion; in addition, there were no changes in RPF, GFR, BP, and plasma aldosterone concentration. The mechanism of the antinatriuresis remains unclear. However, the fact that SQ20881 administration decreased sodium excretion is consistent with the hypothesis that endogenous AII is tonically active in the brain to stimulate sodium excretion.
|Original language||English (US)|
|Number of pages||6|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - Apr 1982|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)