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Endocrinology, doi:10.1210/endo-128-1-204
Endocrinology Vol. 128, No. 1 204-210
Copyright © 1991 by the Endocrine Society.
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Role of Endogenous Angiotensin II in the Control of Vasopressin Secretion during Hypovolemia and Hypotension in Conscious Rabbits*

SHIGEAKI MATSUKAWA, LANNY C. KEIL and IAN A. REID

Department of Physiology, University of California San Francisco, California 94143
Ames Research Center Moffett Field, California 94035

Address all correspondence and requests for reprints to: Dr. Ian A. Reid, Department of Physiology, Box 0444, University of California, San Francisco, California 94143-0444.

Abstract

In order to investigate the physiological role of angiotensin II (ANG II) in the control of vasopressin (VP) secretion, the VP responses to hypotension induced by hemorrhage (20 ml/kg, n = 10) or nitroprusside infusion (1–10 Mg/kgmin, n = 9) were studied with or without blockade of ANG II formation by the converting enzyme inhibitor captopril in conscious rabbits. Administration of captopril (5 mg/kg, iv) caused a small decrease in mean arterial pressure but did not enhance the hypotensive response to subsequent hemorrhage or nitroprusside infusion. The renin response to both stimuli was enhanced by captopril, whereas the increase in plasma ANG II concentration was attenuated. Plasma VP (PAVP) concentration increased during hemorrhage (2.0 ± 0.2-113.6 ± 47.7 pg/ ml, P < 0.01) and nitroprusside infusion (2.1 ± 0.3-5.1 ± 1.0 pg/ ml, P < 0.01). Captopril did not change basal plasma PAVP, nor did it attenuate the VP responses to hemorrhage or nitroprusside. Indeed, captopril tended to enhance the VP responses to hemorrhage (2.3 ± 0.3-147.1 ± 65.9 pg/ml) and nitroprusside infusion (1.9 ± 0.2-15.4 ± 6.0 pg/ml). The relationship between log PAVP and mean arterial pressure during hemorrhage and nitroprusside infusion in the presence of captopril was not different than in the absence of captopril. These results indicate that in conscious rabbits, the renin-angiotensin system does not contribute to the increase in VP secretion during hypotension induced by hemorrhage or nitroprusside infusion. (Endocrinology 128: 204–210, 1991)

Footnotes

* This research was supported by NIH Grant HL-29714.

Received July 9, 1990.




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Copyright © 1991 by The Endocrine Society