A balance between circulating and locally released vasoconstrictors, such as endothelin-1 (ET-1), and vasodilators, such as nitric oxide, controls vascular smooth muscle tone. In the study reported here, using the technique of simultaneous measurements of intracellular free calcium ([Ca2+]i) and tension, we investigated the effects of a nitric oxide donor, sodium nitroprusside (NaNP) on endothelin-1- and U46619- [a thromboxane angiotensin-II (TXA-II) mimetic] induced sustained increases in tension and [Ca2+]i in intact and endothelium-denuded rabbit thoracic aortas. Our results showed that, in both intact and endothelium-denuded preparations, the nitric oxide donor NaNP (10-6 M) reverses the ET-1- (10-7 M) and U46619- (10-7 M) induced sustained increase in tension but not in [Ca2+]i. However, it did not reduce the ET-1- and U46619-induced responses. Our data suggest that nitric oxide production modulates vascular smooth muscle tension via a mechanism that is independent of that generated by vasoconstrictors such as ET-1 and TXA-II.
CIHR group in Immuno-Cardiovascular Interactions, *Department of Anatomy and Cell Biology, and †Department of Pharmacology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Québec, Canada
Address correspondence and reprint requests to Ghassan Bkaily, CIHR group in Immuno-Cardiovascular Interactions, Department of Anatomy and Cell Biology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Québec, Canada, J1H 5N4. E-mail: [email protected]
© 2000 Lippincott Williams & Wilkins, Inc.