The present study was undertaken to determine whether ethanol influences on the agonist-induced vascular smooth muscle contraction and, if so, to investigate the related mechanism. The measurement of isometric contractions using a computerized data acquisition system was combined with molecular experiments. Ethanol significantly inhibited thromboxane A2 mimetic-induced contraction with intact endothelial function, but there was no relaxation on thromboxane A2 mimetic U-46619-induced contraction irrespective of endothelium suggesting that the pathway such as Rho-kinase activation, Ca(2+) entry or thin filament regulation was not affected. In addition, ethanol didn't decrease thromboxane A2 mimetic-induced increase of phospho-myosin phosphatase targeting subunit protein 1 (pMYPT1) or pERK1/2. Interestingly, ethanol didn't inhibit significantly phorbol ester-induced contraction in denuded muscles suggesting that thin filament regulation is less important on the ethanol-induced regulation in the muscle than endothelial NO synthesis. In conclusion, this study provides the evidence and possible related mechanism concerning the effect of ethanol on the agonist-dependent contraction in rat aortic rings with regard to endothelial function.
Keywords: Ethanol; Phorbol ester; Rho-kinase; Thromboxane A2 mimetic; Vasodilation.