Mechanisms of altered sodium excretion after preoptic hypothalamic lesions

S. L. Bealer, Robert William Caldwell, E. Songu-Mize

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Abstract

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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume254
Issue number1
StatePublished - Jan 1 1988
Externally publishedYes

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Natriuresis
Sodium
Aldosterone
Renin
Blood Pressure
Third Ventricle
Bradycardia
Corticosterone
Arterial Pressure
Heart Rate
Urine

ASJC Scopus subject areas

  • Physiology

Cite this

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abstract = "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.",
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