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Am J Physiol Heart Circ Physiol 258: H1655-H1659, 1990;
0363-6135/90 $5.00
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AJP - Heart and Circulatory Physiology, Vol 258, Issue 6 1655-H1659, Copyright © 1990 by American Physiological Society

ARTICLES

Centrally administered ANF promotes appearance of a circulating sodium pump inhibitor

E. Songu-Mize, S. L. Bealer and A. I. Hassid
Department of Pharmacology, College of Medicine, University of Tennessee, Memphis 38163.

We have previously reported that release of an endogenous Na pump inhibitor, a putative natriuretic hormone associated with many hypertensive states, may be regulated by the central nervous system (CNS). The atrial natriuretic factor (ANF), which causes diuresis, vasorelaxation, and inhibition of aldosterone and vasopressin release, has been documented in the CNS as well as the atria and peripheral blood. Our experiments investigate the possible interaction of ANF with a circulating specific inhibitor of the Na pump in normal rats. The Na pump inhibitory capacity of plasma from rats previously injected with either [Arg101-Tyr126]ANF or vehicle into the lateral cerebral ventricle was measured in cultured aortic smooth muscle cells (ASMC) using 86Rb uptake methodology. Plasma from rats injected with ANF inhibited the Na pump activity (18 +/- 4%, n = 4 experiments) in ASMC compared with plasma obtained from rats injected with the vehicle. The nonspecific 86Rb uptake was not affected by the ANF treatment. Plasma obtained from rats injected intravenously with ANF did not affect the Na pump activity in the ASMC. Furthermore, ANF did not directly affect Na pump activity in ASMC when added to the culture dishes in vitro. These findings raise the possibility that central ANF regulates the release of circulating Na pump inhibitor.


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