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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.

Original publication




Journal article


Br J Pharmacol

Publication Date





191 - 193


15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid, Acetylcholine, Animals, Drug Interactions, Endothelium, Vascular, Enzyme Inhibitors, In Vitro Techniques, Male, Membrane Potentials, Mesenteric Artery, Superior, Muscle Contraction, Muscle Relaxation, Muscle, Smooth, Vascular, NG-Nitroarginine Methyl Ester, Nifedipine, Nitric Oxide Synthase, Nitroarginine, Norepinephrine, Prostaglandin Endoperoxides, Synthetic, Rats, Rats, Wistar, Stimulation, Chemical, Thromboxane A2, Vasoconstrictor Agents, Vasodilator Agents