Mechanism of inhibitory action of ethanol on endothelium-dependent relaxation in rat aorta

• Published in: European journal of pharmacology Vol. 238; no. 2; pp. 441 - 444
• Main Authors: Hatake, Katsuhiko, Wakabayashi, Ichiro, Hishida, Shigeru
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 20.07.1993; Elsevier
• Subjects: Acetylcholine; Acetylcholine - pharmacology; Alcoholism and acute alcohol poisoning; Animals; Aorta; Aorta, Thoracic - drug effects; Aorta, Thoracic - physiology; Arginine - analogs & derivatives; Arginine - pharmacology; Biological and medical sciences; Calcimycin - pharmacology; Cyclic GMP - metabolism; Endothelium; Endothelium, Vascular - drug effects; Ethanol; Ethanol - pharmacology; In Vitro Techniques; Male; Medical sciences; Muscle Relaxation - drug effects; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - physiology; Nitric Oxide - physiology; Nitroarginine; Nitroprusside - pharmacology; Rat; Rats; Rats, Wistar; Toxicology; Vasorelaxation; Aorta; Acetylcholine; Ethanol; Rat; Vasorelaxation; Endothelium; Rodentia; 3',5'-GMP; Smooth muscle; In vitro; Parasympathomimetic; Relaxation; Vertebrata; Mammalia; Animal; Blood vessel; Circulatory system; Endothelium derived relaxing factor; Inhibition; Mechanism of action
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/0014-2999(93)90883-J

Using isolated rat aortic strips, we investigated the inhibitory effect of ethanol on endothelium-dependent relaxation induced by acetylcholine, especially on the mediated by endothelium-derived relaxing factor. Ethanol depressed the relaxation induced by acetylcholine and inhibited the increase in the content of intravascular cyclic GMP induced by acetylcholine, but not that induced by sodium nitroprusside or calcimycin. Ethanol also inhibited the acetylcholine-induced relaxation resistant to nitro-L-arginine. These results suggest that ethanol can inhibit the cyclic GMP-dependent relaxation mediated by endothelium-derived relaxing factor. Furthermore, ethanol seems to depress the cyclic GMP-independent relaxation mechanism.