Association of alcohol and hypertensive disease - adapted from the New England Journal of Medicine,

Date: Oct, 1995

Although alcohol consumption is associated with an increased incidence of hypertension and stroke, the mechanism for this effect is unclear. Animal research suggests that alcohol may activate the sympathetic nervous system and the production of corticotropin-releasing hormone. To test this hypothesis, Randin and colleagues evaluated the effect of alcohol on the sympathetic nervous system.

Blood pressure, heart rate and sympathetic nerve action potentials were measured in nine healthy subjects before, during and after an intravenous infusion of alcohol. Each subject received two infusions of alcohol preceded by either dexamethasone or placebo.

The alcohol infusion that was administered after placebo significantly increased the rate of sympathetic discharge from a mean of 16 bursts per minute to a mean of 30 bursts per minute. This increase was followed by a significant increase in the mean arterial pressure (10 mm Hg). Following dexamethasone administration, alcohol infusion did not have an appreciable effect on sympathetic discharge, and the mean arterial pressure decreased 7 mm Hg.

The authors conclude that alcohol-induced sympathetic stimulation, which is centrally mediated, increases arterial blood pressure.

In an accompanying editorial, Victor and Hansen note that light to moderate drinking is associated with increased serum concentrations of high-density lipoprotein cholesterol and a 30 percent reduction in the relative risk of fatal and nonfatal coronary heart disease. Although heavy drinking may cause cardiovascular complications by provoking short-term increases in blood pressure and platelet aggregation, in the absence of illness related to alcohol use, the consumption of one or two drinks per day still seems a safe and advisable practice. (New England Journal of Medicine, June 29,1995, vol.332, pp.1733, 1782.)

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