Hypertension, Vol 21, 939-943, Copyright © 1993 by American Heart Association
RK Davda, LJ Chandler, FT Crews and NJ Guzman
Chronic ethanol consumption is associated with an increased prevalence of
hypertension. The mechanisms of this form of hypertension are unknown. Rats
fed ethanol for 2 days develop a tolerance to the acute vasoconstrictive
effects of ethanol that is believed to be endothelium dependent. We
investigated the effects of acute and chronic ethanol exposure on
agonist-stimulated nitric oxide synthase activity in bovine pulmonary
artery endothelial cells. Exposure of bovine pulmonary artery endothelial
cells to ethanol (100 mmol/L) for 20-120 minutes did not change either
basal or agonist-stimulated nitric oxide synthase activity measured as the
rate of conversion of [3H]L-arginine to [3H]L- citrulline. Chronic exposure
of endothelial cells to ethanol (100 mmol/L) for 96 hours significantly
increased bradykinin-, adenosine 5'- triphosphate-, and
ionomycin-stimulated nitric oxide synthase activity without affecting basal
enzyme activity. The ethanol-induced increase in nitric oxide synthase
response to agonists was dependent on the duration of ethanol exposure as
well as the concentration of ethanol. Moreover, the effect of ethanol was
characterized by an increase in the maximal nitric oxide synthase response
to adenosine 5'-triphosphate without changes in the EC50. Removal of
calcium or addition of N omega- nitro-L-arginine completely abolished
agonist-stimulated nitric oxide synthase activity in both control and
ethanol-treated cells. Our observations support the hypothesis that ethanol
enhances nitric oxide synthase response to agonists during early ethanol
exposure and may serve in a protective role against its hypertensive
effect.
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Ethanol enhances the endothelial nitric oxide synthase response to agonists
Division of Nephrology, Hypertension and Transplantation, University of Florida College of Medicine, Gainesville.
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