Mechanisms of altered sodium excretion after preoptic hypothalamic lesions

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 μeq/h), compared with control-operated (control: 2± 4 mmHg, -14 ± 18 beats/min, 89 ± 34 μeq/h) and unanesthetized control (UC) animals (-1 ± 3 mmHg, -5 ± 12 beats/min, 74 ± 25 μeq/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.