Ethanol affects sympathetic cotransmission and endothelium-dependent relaxation in the rat

The influence of ethanol on sympathetic nerve-mediated contractions of rat tail arteries and on endothelium-dependent relaxation of rat mesenteric arteries by acetylcholine was examined using the method of in vitro pharmacology. Ethanol potentiated sympathetic nerve-mediated contractions. Ethanol had no effect on the neurogenic contractions that remained after alpha-adrenoceptor blockade by prazosin. However, after P2x-purinoceptor desensitisation, the residual nerve-mediated contractions were significantly enhanced by ethanol. Contractions to exogenous noradrenaline and alpha,beta-methylene ATP were unaffected by ethanol. It is concluded that ethanol selectively potentiates the noradrenergic component of sympathetic neurotransmission. Ethanol depressed the relaxation by acetylcholine but not that induced by sodium nitroprusside. These results indicate that ethanol can affect both the neural and endothelial control of vascular tone. The potentiated noradrenergic vasoconstrictor response to sympathetic nerve stimulation and the compromised capacity of the endothelium to cause relaxation after ethanol treatment may contribute to the development of vascular diseases associated with alcohol consumption.