AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 257: H502-H505, 1989;
0363-6135/89 $5.00
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AJP - Heart and Circulatory Physiology, Vol 257, Issue 2 502-H505, Copyright © 1989 by American Physiological Society


ARTICLES

Mechanism mediating hypotensive effect of ANF in sodium-depleted dogs

J. P. Granger, E. Meadows, S. Sooudi and D. L. Stacy
Department of Physiology, Eastern Virginia Medical School, Norfolk 23501.

Previous studies have indicated that suppression of renin release and antagonism of the vasoconstrictor actions of angiotensin II (ANG II) may be important mechanisms whereby atrial natriuretic factor (ANF) decreases arterial pressure (AP). The objective of this study was to determine the importance of renin suppression and ANG II antagonism in mediating the hypotensive effects of ANF in Na-depleted, high-renin dogs. Infusion of ANF (300 ng.kg-1.min-1) for 45 min in Na-depleted dogs decreased plasma renin activity (PRA) from 7.5 +/- 2.3 to 3.1 +/- 1.1 ng ANG I.ml-1.h-1. Associated with this fall in PRA was a significant reduction in AP and total peripheral resistance (TPR). Although cardiac output (CO) tended to fall, statistically significant reductions in CO (2.11 +/- 0.19 vs. 1.99 +/- 0.10 l/min) did not occur. In contrast to these findings, infusion of ANF (300 ng.kg-1.min-1) in Na-depleted dogs with fixed circulating levels of ANG II had no significant effect on AP or TPR. Results from this study suggest that renin suppression may be an important mechanism whereby ANF reduces AP in Na-depleted dogs. The results also suggest that antagonism of the vasoconstrictor actions of ANG II is not a potent mechanism whereby ANF decreases AP.





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