Chronic ethanol consumption and hypertension are related. In the current study we investigated whether changes in reactivity of the mesenteric arterial bed could account for the increased blood pressure associated with chronic ethanol intake. Changes in reactivity to phenylephrine and acetylcholine were investigated in the perfused mesenteric bed from rats treated with ethanol for 2 or 6 weeks and their age-matched controls. Mild hypertension was observed in chronically ethanol-treated rats. Treatment of rats for 6 weeks induced an increase in the contractile response of endothelium-intact mesenteric bed to phenylephrine, but not denuded rat mesenteric bed. The phenylephrine-induced increase in perfusion pressure was not altered after 2 weeks' treatment with ethanol. Moreover, acetylcholine-induced endothelium-dependent relaxation was reduced by ethanol treatment for 6 weeks, but not 2 weeks. Pre-treatment with indometacin, a cyclooxygenase inhibitor, reduced the maximum effect induced by phenylephrine (Emax) in endothelium-intact mesenteric bed from both control and ethanol-treated rats. No differences in the Emax values for phenylephrine were observed between groups in the presence of indometacin. L-NNA, a nitric oxide (NO) synthase (NOS) inhibitor, increased the Emax for phenylephrine in endothelium-intact mesenteric bed from control rats but not from ethanol-treated rats. Levels of endothelial NOS (eNOS) mRNA were not altered by chronic ethanol consumption. However, chronic ethanol intake strongly reduced eNOS protein levels in the mesenteric bed. This study shows that chronic ethanol consumption increases blood pressure and alters the reactivity of the mesenteric bed. Moreover, the increased vascular response to phenylephrine observed in the mesenteric bed is maintained by two mechanisms: an increased release of endothelial-derived vasoconstrictor prostanoids and a reduced modulatory action of endothelial NO, which seems to be associated with reduced post-transcriptional expression of eNOS.

This study investigates whether chronic ethanol consumption increases blood pressure and alters vascular reactivity in different tissues. Changes in reactivity to phenylephrine and acetylcholine were investigated in the aorta, carotid artery and mesenteric arterial bed (MAB) isolated from rats pretreated with ethanol for 2 or 6 weeks. Mild hypertension was observed in chronically ethanol-treated rats, which was due to rises in both systolic and diastolic pressures. Chronic ethanol consumption increased the contractile response to phenylephrine of endothelium-intact and denuded rat aortic rings from rats pretreated with ethanol for 2 or 6 weeks. Conversely, no differences were found in acetylcholine-induced relaxation. Neither phenylephrine-induced contraction nor acetylcholine-induced relaxation were altered in the rat carotid. Six weeks' ethanol consumption enhanced the contractile response to phenylephrine of endothelium-intact, but not denuded rat MAB. On the other hand, 2 weeks' ethanol consumption did not affect phenylephrine-induced increase in perfusion pressure. Moreover, acetylcholine-induced endothelium-dependent relaxation in the MAB was reduced after treatment with ethanol for 6 weeks but not after 2 weeks. In conclusion, ethanol affects both blood pressure and vessel reactivity, but the effect on vascular reactivity may take longer to become apparent in MAB than in the aorta, and was not evident in the carotid. Moreover, we provide evidence that the effect of ethanol depends on the agonist and blood vessel studied.

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