Blood pressure and vascular reactivity to endothelin-1, phenylephrine, serotonin, KCI and acetylcholine following chronic alcohol consumption in vitro

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Utkan T. , Yıldız F., Ilbay G. , Ozdemırcı S., Erden B. F. , Gacar N., ...More

FUNDAMENTAL & CLINICAL PHARMACOLOGY, vol.15, pp.157-165, 2001 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 15
  • Publication Date: 2001
  • Doi Number: 10.1046/j.1472-8206.2001.00024.x
  • Page Numbers: 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 responsiveness 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 isocaloric carbohydrate for 4 weeks were placed in organ chambers for isometric tension measurement. There was a mild but significant elevation of the systolic blood pressure in the alcohol-fed rats by week 1 compared to baseline measurements and this remained higher. No significant changes in reactivity of rat isolated aortas to phenylephrine, serotonin, endothelin-1 (ET-1) and KCl were seen in chronic ethanol consumption. In addition, the sensitivity (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 monophosphate (cGmp)-dependent direct smooth muscle dilator. The results indicate that chronic ethanol consumption significantly potentiates endothelium-dependent relaxations in aortic rings, probably through interference with the production 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 for the blood pressure elevation in the chronic alcohol consumption in rats.