Intracerebroventricular Infusions of Angiotensin II Increases Sodium Excretion

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Abstract
The mechanism by which intracerebroventricular administration of angiotensin II (AII) enhances renal Na excretion was studied in anesthetized dogs. Intraventricular infusion of AII (6 ng/min) increased Na 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 [teprotide] (0.5 .mu.g/min), was infused intraventricularly in another group of dogs. This infusion decreased Na 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 Na excretion is consistent with the hypothesis that endogenous AII is tonically active in the brain to stimulate Na excretion.

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