Open AccessNitric Oxide Relaxes the Vascular Smooth Muscle Independently of Endothelin-1- and U46619-Induced Intracellular Increase of Calcium
Author(s) -
Ghassan Bkaily,
Hadia Shbaklo,
Magda Taoudi-Benchekroun,
Sawsan Sader,
Martine Duval,
Danielle Jacques,
Pedro D’Orléans-Juste
Publication year - 2000
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-200036051-00036
Subject(s) - nitric oxide , sodium nitroprusside , vascular smooth muscle , thromboxane a2 , chemistry , vasodilation , endothelin receptor , endocrinology , endothelin 1 , medicine , endothelium derived relaxing factor , endothelium , calcium , vasoconstriction , smooth muscle , platelet , receptor
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.