Influence of contractile agonists on the mechanism of endothelium‐dependent relaxation in rat isolated mesenteric artery
Open Access
- 1 September 1996
- journal article
- Published by Wiley in British Journal of Pharmacology
- Vol. 119 (2), 191-193
- https://doi.org/10.1111/j.1476-5381.1996.tb15970.x
Abstract
This study demonstrates directly that the relative contribution of nitric oxide (NO) and an NO synthase-independent repolarization to acetylcholine-evoked relaxation in rat isolated mesenteric resistance arteries is determined by the processes which mediate pre-contraction. Noradrenaline-induced contractions were reversed by acetylcholine via both NO and NO synthase-independent smooth muscle repolarization. In contrast, reversal of contractions to the thromboxane-mimetic, U46619, by acetylcholine was entirely mediated by the actions of NO, independently of a change in membrane potential.Keywords
This publication has 4 references indexed in Scilit:
- Evidence for mediation by endothelium‐derived hyperpolarizing factor of relaxation to bradykinin in the bovine isolated coronary artery independently of voltage‐operated Ca2+ channelsBritish Journal of Pharmacology, 1996
- Contribution of both nitric oxide and a change in membrane potential to acetylcholine‐induced relaxation in the rat small mesenteric arteryBritish Journal of Pharmacology, 1994
- Evidence that nitric oxide does not mediate the hyperpolarization and relaxation to acetylcholine in the rat small mesenteric arteryBritish Journal of Pharmacology, 1992
- Noradrenaline contracts arteries by activating voltage-dependent calcium channelsNature, 1988