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

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...

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Published inEuropean journal of pharmacology Vol. 238; no. 2; pp. 441 - 444
Main Authors Hatake, Katsuhiko, Wakabayashi, Ichiro, Hishida, Shigeru
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 20.07.1993
Elsevier
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Abstract 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.
AbstractList Using isolated rat aortic strips, we investigated the inhibitory effect of ethanol on endothelium-dependent relaxation induced by acetylcholine, especially on that 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.
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.
Author Wakabayashi, Ichiro
Hishida, Shigeru
Hatake, Katsuhiko
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  fullname: Wakabayashi, Ichiro
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  givenname: Shigeru
  surname: Hishida
  fullname: Hishida, Shigeru
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Issue 2
Keywords 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
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Elsevier
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SubjectTerms 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
Title Mechanism of inhibitory action of ethanol on endothelium-dependent relaxation in rat aorta
URI https://dx.doi.org/10.1016/0014-2999(93)90883-J
https://www.ncbi.nlm.nih.gov/pubmed/8405115
https://search.proquest.com/docview/75997515
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