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The pressor effect of moderate alcohol consumption in man: a search for mechanisms.
Author(s) -
Peter D. Arkwright,
Lawrence J. Beilin,
R. Vandongen,
Ian Rouse,
Claire M. Lalor
Publication year - 1982
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.66.3.515
Subject(s) - medicine , plasma renin activity , blood pressure , supine position , isometric exercise , heart rate , endocrinology , population , cold pressor test , diastole , norepinephrine , renin–angiotensin system , dopamine , environmental health
Thirty pairs of drinking and nondrinking men, matched for age and weight, were drawn from a working population in which a close relationship between alcohol consumption and blood pressure had been demonstrated. In this smaller sample, men who drank an average of 408 ml of ethanol/week had higher supine (126.9 +/- 2.3 mm Hg) and standing (113.3 +/- 2.5 mm Hg) systolic and supine diastolic blood pressure (75.5 +/- 2.2 mm Hg) than nondrinkers (117.5 +/- 2.0, 107.4 +/- 2.2 and 68.9 +/- 1.8 mm Hg, respectively). Resting plasma concentrations of free and sulfated norepinephrine and epinephrine, renin activity, angiotensin II, aldosterone and cortisol were similar in drinkers and nondrinkers. To investigate differences that may arise when sympathoadrenal activity was stimulated, the subjects underwent a series of standardized physiologic stresses: isometric hand grip, mental arithmetic, cold pressor testing, standing and bicycle exercise. Blood pressure and heart rate responses were similar in drinkers and nondrinkers, although the differences in blood pressure between the two groups tended to become smaller after certain stresses. No differences in the plasma levels of free or conjugated catecholamines were apparent after these stresses. Plasma renin activity increased only after bicycle exercise, and this was similar in both groups. Plasma cortisol levels did not increase. The higher blood pressure in drinkers, therefore, cannot be explained by increased activity of the sympathoadrenal and renal pressor mechanisms.

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