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Increased Endothelium‐Dependent Vascular Relaxation in Ethanol‐Fed Rats

Katsuhiko Hatake, Ichiro Wakabayashi, Tadaaki Taniguchi, Shigeru Hishida

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Abstract

We investigated the mechanism underlying increased relaxation of aortic strips to acetylcholine in rats chronically treated with ethanol. Rats were divided into three groups and maintained on liquid diets containing ethanol (35% of total calories) as the ethanol-fed group or an equicaloric volume of sucrose instead of ethanol as the sucrose-fed group for 10 weeks. The control group was also maintained on modified American Institute of Nutrition diet for the same period. Vascular strips of isolated rat aortas were mounted in organ chambers to record isometric tension. The endothelium-dependent relaxation responses to acetylcholine and calcium ionophore A23187 were greater in ethanol-fed rats than in control and sucrose-fed rats. However, the relaxation response to sodium nitroprusside or nifedipine did not differ among the three groups. Acetylcholine, calcium ionophore A23187, and sodium nitroprusside caused an increase in the cGMP contents of rat aortic strips that was similar among the three groups. These results suggest that a cGMP-independent relaxation mechanism is involved in the increased relaxation response to acetylcholine after chronic treatment with ethanol.

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We investigated the mechanism underlying increased relaxation of aortic strips to acetylcholine in rats chronically treated with ethanol. Rats were divided into three groups and maintained on liquid diets containing ethanol (35% of total calories) as the ethanol-fed group or an equicaloric volume of sucrose instead of ethanol as the sucrose-fed group for 10 weeks. The control group was also maintained on modified American Institute of Nutrition diet for the same period. Vascular strips of isolated rat aortas were mounted in organ chambers to record isometric tension. The endothelium-dependent relaxation responses to acetylcholine and calcium ionophore A23187 were greater in ethanol-fed rats than in control and sucrose-fed rats. However, the relaxation response to sodium nitroprusside or nifedipine did not differ among the three groups. Acetylcholine, calcium ionophore A23187, and sodium nitroprusside caused an increase in the cGMP contents of rat aortic strips that was similar among the three groups. These results suggest that a cGMP-independent relaxation mechanism is involved in the increased relaxation response to acetylcholine after chronic treatment with ethanol.

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Available abstract

We investigated the mechanism underlying increased relaxation of aortic strips to acetylcholine in rats chronically treated with ethanol. Rats were divided into three groups and maintained on liquid diets containing ethanol (35% of total calories) as the ethanol-fed group or an equicaloric volume of sucrose instead of ethanol as the sucrose-fed group for 10 weeks. The control group was also maintained on modified American Institute of Nutrition diet for the same period. Vascular strips of isolated rat aortas were mounted in organ chambers to record isometric tension. The endothelium-dependent relaxation responses to acetylcholine and calcium ionophore A23187 were greater in ethanol-fed rats than in control and sucrose-fed rats. However, the relaxation response to sodium nitroprusside or nifedipine did not differ among the three groups. Acetylcholine, calcium ionophore A23187, and sodium nitroprusside caused an increase in the cGMP contents of rat aortic strips that was similar among the three groups. These results suggest that a cGMP-independent relaxation mechanism is involved in the increased relaxation response to acetylcholine after chronic treatment with ethanol.

Key concepts: Endothelium, Ethanol, Relaxation (psychology), Internal medicine, Chemistry, Cardiology, Endocrinology, Medicine

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