Nitric Oxide Relaxes the Vascular Smooth Muscle Independently of Endothelin-1- and U46619-Induced Intracellular Increase of Calcium
- 1 January 2000
- journal article
- vascular effects
- Published by Wolters Kluwer Health in Journal of Cardiovascular Pharmacology
- Vol. 36 (Supplement) , S110-S116
- https://doi.org/10.1097/00005344-200036051-00036
Abstract
Summary: 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 (10-6M) 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 TX-A-II.Keywords
This publication has 0 references indexed in Scilit: