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The BP increase does not seem to be an immediate effect of alcohol.​2,3​ Japanese investigators, as
cited in a review,​3​ used ambulatory monitoring in hypertensives to demonstrate a short-term
depressor effect of a dinner time alcohol dose of 1 mL/kg, with persistence of lower BP for up to
8 hours, but higher pressures the next morning. They also examined morning and late evening
home BP for 4 weeks in a usual alcohol consumption period and for 4 weeks in alcohol
restriction, finding a depressor effect of alcohol on the evening BP from day 1 to week 4, and a
presser effect on the morning BP from week 2 regardless of the order of the 2 periods. These
results suggest a short-term biphasic effect of alcohol on BP. Unfortunately, these ambulatory
monitoring data only involve alcohol with food. The time sequence of the alcohol–BP effect
indicates that higher pressures on Monday do not necessarily represent withdrawal effects.

data indicating that frequency of drinking may be more important than amount or beverage
choice as a predictor of lower coronary risk.

For those who choose to be light-to-moderate drinkers, a US government guideline advises "take
with meals to slow alcohol absorption

To minimize risks and maximize benefit of light/moderate consumption of alcohol, a small

amount most days with meals is the way to go.

Although alcohol influences both systolic and diastolic pressures, its


effect on systolic pressure appears to be greater (Table 1). Men are more sensitive to the
hypertensive effects of alcohol than women

Between one-third and one-half of persons undergoing alcohol detoxification will manifest

The reaction to stress in this experiment was measured by a cold pressor test, in which the
subject's hand is plunged into ice water for 1 minute and blood pressure subsequently monitored
at 30-second intervals.

elevated blood concentrations of only two of them--cortiso (Bannnan et al. 1984) and
epinephrine (Clark and Friedman 1985)--have been related to hypertension during withdrawal,
and even these associations are not strong.

In one study, male rats given 20-percent alcohol in their drinking water exhibited an elevation of
blood pressure after 4 weeks of treatment (Chan and Sutter 1983). In these animals, urinary
volume and urinary sodium concentratoin decreased while blood volume and blood
norepinephrine concentration increased. The blood pressure and norepinephrine responses were
further enhanced by exposure to stress (in the form of 30 minutes of heat radiation). These
results suggest that alcohol may influence blood pressure by affecting the production, by the
nervous system, kidneys, or adrenal glands, of hormones related to water balance or arterial

It is also possible that alcohol affects vascular constriction by acting directly on the muscle
layers of the vessel walls. Low concentrations of alcohol are known to inhibit spontaneous
contraction of isolated vascular muscle tissu; these effects, which theoretically would tend to
decrease blood pressure, may be expected to occur in humans after a single drink of 1 ounce to 2
ounces of alcohol (Altura and Altura 1987). Upon further exposure to alcohol, blood vessels
progressively regain their contractility, indicating the development of tolerance to this inhibitory
effect. If vascular responsiveness continues to increase as alcohol exposure becomes chronic,
blood pressure would ultimately tend to increase.

These changes in vascular responsiveness were associated with an increase in the content of
calcium and a decrease of magnesium in the strips.

Calcium is required for contraction, while magnesium encourages vascular relaxation by

regulating the uptake, content, and distribution of calcium in the muscle cells