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SAMUEL A. MALAYAN, LANNY C. KEIL, DAVID J. RAMSAY, IAN A. REID, Mechanism of Suppression of Plasma Renin Activity by Centrally Administered Angiotensin II, Endocrinology, Volume 104, Issue 3, 1 March 1979, Pages 672–675, https://doi.org/10.1210/endo-104-3-672
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Experiments were performed to determine if the suppression of plasma renin activity (PRA) produced by injection of angiotensin II into the cerebral ventricles is a consequence of the associated increase in plasma vasopressin concentration or arterial blood pressure. The possibility that vasopressin mediates the pressor effect of centrally administered angiotensin II was also investigated. The experiments were performed in pentobarbital- anesthetized dogs with cannulas placed in the third cerebral ventricle. Thirty min after intraventricular injection of angiotensin II (500 ng) in 12 dogs, PRA decreased from 16.0 ± 3.7 to 12.0 ± 3.5 ng/ml-3 h (P < 0.05) in association with an increase in plasma vasopressin concentration from 9.7 ± 1.8 to 20.4 ± 3.6 pg/ml (P < 0.001) and an increase in mean arterial pressure from 124 ± 4 to 136 ± 5 mm Hg (P < 0.001). In 9 acutely hypophysectomized dogs, intraventricular angiotensin II produced no changes in PRA (37.3 ± 8.6 to 35.1 ± 7.4 ng/ml-3 h) or plasma vasopressin concentration (2.5 ± 0.3 to 2.7 ± 0.2 pg/ml) but increased mean arterial pressure from 103 ± 5 to 112 ± 6 mm Hg (P < 0.001). The increase in arterial pressure produced by intraventricular angiotensin II in the hypophysectomized dogs was not significantly different from that in the intact dogs. These results demonstrate that the decrease in PRA produced by intraventricular angiotensin II is not due to the increase in arterial pressure but is probably due to the increase in plasma vasopressin concentration. The data also indicate that the pressor effect of intraventricular angiotensin II is not due to stimulation of vasopressin release.
