AJP - Regulatory, Integrative and Comparative Physiology, Vol 254, Issue 1 84-R89, Copyright © 1988 by American Physiological Society

ARTICLES

Mechanisms of altered sodium excretion after preoptic hypothalamic lesions

S. L. Bealer, R. W. Caldwell and E. Songu-Mize
Department of Physiology and Biophysics, University of Tennesse, Memphis 38163.

These experiments investigated cardiovascular and hormonal responses during the natriuresis and subsequent sodium retention following electrolytic lesions of the periventricular tissue surrounding the anteroventral third ventricle (AV3V-X) in the rat. Four hours following treatment, AV3V-X resulted in a significant increase in blood pressure (18 +/- 3 mmHg), bradycardia (-68 +/- 20 beats/min), and natriuresis (212 +/- 36 mu eq/h), compared with control-operated (control: 2 +/- 4 mmHg, -14 +/- 18 beats/min, 89 +/- 34 mu eq/h) and unanesthetized control (UC) animals (-1 +/- 3 mmHg, -5 +/- 12 beats/min, 74 +/- 25 mu eq/h). Preventing the hypertensive response in AV3V-X rats abolished the natriuresis. Twenty-four hours after treatment, blood pressure, heart rate, urine flow, and sodium excretion were similar between experimental groups. However, sodium excretion by AV3V-X rats was significantly smaller than control 24-48 h following treatment. AV3V-X rats had significantly elevated plasma concentrations of aldosterone and corticosterone 4, 24, and 48 h and increased plasma renin 24 and 48 h after treatment. These data suggest that the acute natriuresis following AV3V-X is mediated by increased arterial blood pressure, whereas the subsequent sodium retention could be due to activation of the renin-aldosterone system.

This article has been cited by other articles:

				D. S. A. Colombari and S. L. Cravo Effects of Acute AV3V Lesions on Renal and Hindlimb Vasodilation Induced by Volume Expansion Hypertension, October 1, 1999; 34(4): 762 - 767. [Abstract] [Full Text] [PDF]