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Am J Physiol Cell Physiol 271: C923-C928, 1996;
0363-6143/96 $5.00
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AJP - Cell Physiology, Vol 271, Issue 3 C923-C928, Copyright © 1996 by American Physiological Society

ARTICLES

Thrombin-induced vascular reactivity is modulated by ETB receptor-coupled nitric oxide release in rat aorta

H. I. Magazine and K. D. Srivastava
Department of Biology, Queens College, Flushing, New York, USA.

The role of endothelin (ET) receptors in thrombin-induced modulation of vascular tone was evaluated by direct measurement of ET-1 and ET receptor-coupled nitric oxide (NO) release and developed isometric tension in thrombin-treated aortic rings. Here we report that rapid release of ET-1 and subsequent ETB receptor activation are required for production of the potent vasodilator NO by thrombin-stimulated aorta. Thrombin-induced NO release is ablated by pretreatment with ETB receptor antagonists or after ET receptor desensitization by repeated stimulation with ET-1. Thrombin-induced relaxation of precontracted vessels was abrogated in the presence of ETB receptor antagonists and, in contrast, marked contraction to thrombin was observed. These data indicate that the endothelium-dependent vasodilator activity previously attributed to thrombin is indirect and requires ETB receptor-coupled NO release and suggest that ET receptor modulation of thrombin-induced vascular tone may contribute to the increased vasomotor tone observed in diseased and mechanically injured vessels.


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