Potential Mechanisms of Effect on BP
Several mechanisms have been proposed for the relationship between alcohol and elevated BP. An immediate effect of alcohol ingestion is vasodilation in some vascular beds. Sustained intake accompanied by high blood alcohol levels, however, results in short-term elevation of BP.  In addition, BP levels usually correlate best with alcohol intake within the prior 24 hours, and fall within hours to days after cessation or reduction in intake. [13,14] Therefore, it is likely that the effect of alcohol on BP is not mediated by long-term structural alterations, but by neural, hormonal, or other reversible physiologic changes.
According to one hypothesis, the hypertensive effect of alcohol is from a chronic state of alcohol withdrawal in frequent, heavy drinkers, but there is much evidence in favor of a direct effect of alcohol on BP. Suggested mediators of a direct effect include: 1) stimulation of the sympathetic nervous system, endothelin, renin-angiotensin-aldosterone system, insulin (or insulin resistance), or cortisol; 2) inhibition of vascular relaxing substances, e.g., nitric oxide; 3) calcium or magnesium depletion; 4) increased intracellular calcium or other electrolytes in vascular smooth muscle, possibly mediated by changes in membrane electrolyte transport; and 5) increased acetaldehyde. [31,32,33] There appears to be more evidence to support the role of the sympathetic nervous system or cellular transport and electrolytes, or both, than the other mechanisms suggested, but this remains an open question.
© 2001 Le Jacq Communications, Inc.
Cite this: Alcohol Consumption and Hypertension - Medscape - May 01, 2001.