Nitric oxide relaxes the vascular smooth muscle independently of endothelin-1-and U46619-induced intracellular increase of calcium

A balance between circulating and locally released vasoconstrictors, such a s endothrlin-1 (ET-1), and vasodilators, such as nitric oxide, controls vas cular smooth muscle tone. In the study reported here, using the technique o f simultaneous measurements of intracellular free calcium ([Ca2+]i) and ten sion, we investigated the effects of a nitric oxide donor, sodium nitroprus side (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 N aNP (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 redu ce the ET-1- and U46619-induced responses. Our data suggest that nitric oxi de production modulates vascular smooth muscle tension via a mechanism that is independent of that generated by vasoconstrictors such as ET-1 and TXA- II.