抄録
Variant form of angina pectoris is known to be induced sometimes by alcohol ingestion. The author reported that patients attacked by alcoholinduced coronary spasm there was an association with a gradual decrease of cyclic GMP levels in the plasma before the induction of attack. To investigate the mechanism of alcohol-induced coronary spasm, we conducted an in vitro study on the effect of alcohol on cyclic GMP metabolism, using cultured smooth muscle cells isolated from porcine coronary artery.
The effects of ethanol and its metabolite, acetaldehyde, on guanylate cyclase activity and cyclic GMP were studied with or without sodium nitroprusside (SNP).
Ethanol at the concentration of 4.0mg/m/ was found to suppress guanylate cyclase activity. Enhanced accumulation of cyclic GMP by SNP was inhibited by a similar concentration of etha nol, whereas the basal level of cyclic GMP was suppressed by a concentration of 12mg/m/ or more. Acetaldehyde also showed both suppression of guanylate cyclase activity and inhibition of cyclic GMP accumulation, though it required rather high concentration to exert these eflects.
Cyclic GMP is known as a key substance in vasodilatation by endothelium-derived relaxing factor, atrial natriuretic factors and nitrovasodilators. The results of our in vitro study suggests that the effects of ethanol on cyclic GMP metabolism in smooth muscle cell could play an important role on ethanol-induced vasospastic angina.
