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Am J Physiol Regul Integr Comp Physiol 257: R194-R203, 1989;
0363-6119/89 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 1 194-R203, Copyright © 1989 by American Physiological Society

ARTICLES

Mechanism of inhibition of renin response to hypotension by atrial natriuretic factor

D. A. Scheuer, T. N. Thrasher, L. C. Keil and D. J. Ramsay
Department of Physiology, University of California, San Francisco 94143-0444.

We have reported that infusion of atrial natriuretic factor (ANF) inhibited the rise in plasma renin activity (PRA) in response to constriction of the abdominal aorta to cause a reduction in renal perfusion pressure (RPP). To evaluate the effect of ANF on neural control of renin release, acute thoracic inferior vena caval constriction (TIVCC) was performed in conscious dogs to reduce arterial pressure by 25% of control and stimulate PRA by a reflex increase in renal nerve activity and a reduction in RPP. Propranolol was used to block neural stimulation of renin release. TIVCC caused significant increases in PRA, plasma aldosterone, arginine vasopressin (AVP), and adrenocorticotropic hormone (ACTH) concentrations. The increase in PRA was significantly reduced by the infusion of either ANF at 20 ng.kg-1.min-1 or propranolol. The combined infusion of ANF and propranolol produced an additive and complete inhibition of the renin response to TIVCC; therefore the effect of ANF is independent of neural stimulation of renin release. ANF at 20 ng.kg-1.min-1 also inhibited increases in aldosterone, AVP, and ACTH, but ANF at 5 ng.kg-1.min-1 only affected the aldosterone response to TIVCC. Therefore ANF inhibits angiotensin II-stimulated aldosterone synthesis and/or secretion at very low doses and at higher doses attenuates reflex increases in AVP and ACTH caused by hypotension.


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[Abstract] [Full Text] [PDF]


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