Hypertension, Vol 13, 964-967, Copyright © 1989 by American Heart Association
L Criscione, JR Powell, R Burdet, S Engesser, F Schlager and A Schoepfer
The effects of prolonged infusions of ethanol on endothelium-dependent
vasorelaxation induced by acetylcholine and adenosine triphosphate (ATP)
and on endothelium-independent relaxation induced by papaverine were
studied and compared in isolated perfused rat mesenteric artery
preparations. Infusion of ethanol over 60 minutes at concentrations of 1.6,
4.7, 6.3, and 7.9 mg/ml caused concentration-related inhibition of
norepinephrine-induced vasoconstriction. In preparations infused with 6.3
and 7.9 mg/ml, this effect reached a maximum after 10-20 minutes but had
vanished by the end of the infusion; 1 hour after the end of the infusion,
the effects of norepinephrine were potentiated by 71% and 108%,
respectively. Acetylcholine-induced vasorelaxation (EC50 3.0 ng/ml in
controls) was significantly reduced after 6.3 mg/ml ethanol infusion and
totally abolished after 7.9 mg/ml ethanol infusion. ATP- induced
vasorelaxation (EC50 180 ng/ml in controls) was also abolished after 7.9
mg/ml of ethanol infusion. By contrast, the vasorelaxant effects of
papaverine were not affected by 7.9 mg/ml ethanol infusion.
Light-microscopic examination revealed that the endothelial cells were
present in ethanol-treated and in control mesenteric arterial beds. These
observations indicate that ethanol suppresses endothelium- dependent
vasorelaxation without apparent removal of the endothelial cells. The
compromised relaxant capacity of the endothelium after ethanol and the
resultant intensification of the vasoconstrictor response to norepinephrine
may contribute to the development of vascular diseases such as hypertension
and stroke.
ARTICLES
Alcohol suppresses endothelium-dependent relaxation in rat mesenteric vascular beds
Cardiovascular Research Department, CIBA-GEIGY Ltd., Basel, Switzerland.
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