T. Utkan et al., Blood pressure and vascular reactivity to endothelin-1, phenylephrine, serotonin, KCI and acetylcholine following chronic alcohol consumption in vitro, FUN CL PHAR, 15(3), 2001, pp. 157-165
Ethanol has been reported to cause hypertension, the mechanism of which is
unknown. Therefore, the effect of chronic ethanol consumption on vascular r
esponsiveness and blood pressure was investigated. Systolic blood pressure
was recorded weekly by tail-cuff method. Aortic rings from rats fed chow ad
libitum or pair-fed liquid diets containing either ethanol (7.2% v/v) or i
socaloric carbohydrate for 4 weeks were placed in organ chambers for isomet
ric tension measurement. There was a mild but significant elevation of the
systolic blood pressure in the alcohol-fed rats by week 1 compared to basel
ine measurements and this remained higher. No significant changes in reacti
vity of rat isolated aortas to phenylephrine, serotonin, endothelin-1 (ET-1
) and KCl were seen in chronic ethanol consumption. In addition, the sensit
ivity (i.e. pD(2)) of alcohol-fed aortic rings to the vaso constrictors was
also unchanged compared to controls. Chronic ethanol consumption, however,
increased relaxation to acetylcholine with increased pD(2) values, but did
not alter relaxation to sodium nitroprusside, a cyclic guanosine monophosp
hate (cGmp)-dependent direct smooth muscle dilator. The results indicate th
at chronic ethanol consumption significantly potentiates endothelium-depend
ent relaxations in aortic rings, probably through interference with the pro
duction and/or the release of nitric oxide (NO) or adaptive alterations in
muscarinic receptors on the endothelial cells, and that increased vascular
responsiveness to several vasoconstrictors is not a mechanism responsible f
or the blood pressure elevation in the chronic alcohol consumption in rats.