Alcohol stimulation of renin release in man: its relation to the hemodynamic, electrolyte, and sympatho-adrenal responses to drinking

• Published in: The journal of clinical endocrinology and metabolism Vol. 61; no. 1; p. 37
• Main Authors: Puddey, I B, Vandongen, R, Beilin, L J, Rouse, I L
• Format: Journal Article
• Language: English
• Published: United States 01.07.1985
• Subjects: Adult; Blood Glucose - metabolism; Blood Pressure - drug effects; Diuresis - drug effects; Epinephrine - blood; Ethanol - blood; Ethanol - pharmacology; Hemodynamics - drug effects; Humans; Kinetics; Male; Norepinephrine - blood; Potassium - metabolism; Renin - blood; Renin-Angiotensin System - drug effects; Sodium - metabolism; Sympathetic Nervous System - drug effects; Water-Electrolyte Balance - drug effects
• ISSN: 0021-972X
• DOI: 10.1210/jcem-61-1-37

Alcohol stimulation of the renin-angiotensin axis has been proposed as an explanation for the higher blood pressure in drinkers. This study examines the acute effects of moderate alcohol intake on PRA in relation to change in fluid and electrolyte balance, sympatho-adrenal activity, blood pressure, and heart rate in 20 normal men, aged 20-24 yr. They consumed either 750 ml nonalcoholic beer as a control or the same beverage with 1 ml/kg alcohol added, which increased the plasma alcohol concentration to 16.7 +/- 1.0 (+/- SE) mM within 70 min. PRA increased more than 2-fold 90 min after the ingestion of alcohol. This was accompanied by a decrease in diastolic blood pressure and a fall in plasma potassium, both possible stimuli to the rise in PRA. A late increase in plasma sodium, also occurring 90 min after alcohol ingestion, was attributed to plasma volume contraction after an alcohol-induced diuresis. This may have been an additional factor in stimulating renin release. Norepinephrine levels increased during both alcohol and control studies. In contrast, plasma epinephrine decreased significantly during the control study, but did not change after alcohol ingestion. Hence, alcohol stimulation of sympathetic nervous activity is unlikely to have mediated the renin release. We conclude that the acute increase in PRA associated with moderate alcohol consumption is predominantly a secondary response to changes in fluid and electrolyte balance and blood pressure. Although a direct action of alcohol on renin release was not excluded, the possibility that repeated activation of the renin-angiotensin system mediates the pressor effect of regular moderate alcohol consumption is, therefore, diminished.