Chronic Alcohol Intake Induces Reversible Disturbances on Cellular Na⁺ Metabolism in Humans: Its Relationship with Changes in Blood Pressure

Abstract

The effect of chronic alcohol consumption on Na(+)-K+ ATPase, Na(+)-Li+ countertransport, outward Na(+)-K(+)-Cl- cotransport system and the Na+ leak was investigated in red blood cells from 18 normotensive subjects with a daily alcohol intake of more than 150 g. The study was repeated after 3 months of alcohol withdrawal, and results were compared with a group of 20 healthy normotensive teetotalers. Maximal efflux rate (Vmax) and apparent dissociation constant for internal Na+ (KNa) of the Na(+)-K+ pump and the Na(+)-Li+ countertransport were significantly higher in alcohol consumers. A positive correlation between daily alcohol intake and Vmax of both transport systems (p less than 0.05) was observed. These values significantly decreased after alcohol withdrawal. A simultaneous stimulation of the Na(+)-K(+)-Cl- cotransport system after alcohol withdrawal was also observed. Blood pressure values were higher in alcoholics (133.7/82.3) than in abstainers (121.4/75 mmHg) and significantly decreased (128.5/76.9 mmHg) after withdrawal. A positive correlation between the stimulation of the Na(+)-K(+)-Cl- cotransport and the decrease of blood pressure after withdrawal was observed. In conclusion, chronic alcohol intake induces disturbances on red blood cell Na+ metabolism that dissipate with the cessation of drinking. Similar abnormalities also reported in humans and animals with primary hypertension have been associated in the pathogenesis of essential hypertension. Therefore, the pressor effect of chronic alcohol intake could be mediated through these changes in cellular Na+ metabolism.

Effects of Antihypertensive Drugs on Alcohol-Induced Functional Responses of Cultured Human Endothelial Cells

“…Although the link between alcohol and hypertension has been investigated extensively, a clear mechanism for the pressor effects of ethanol has not yet been established. Past studies have linked the effects of chronic alcohol consumption to activation of the sympathetic nervous system (25,26), stimulation of the renin-angiotensin-aldosterone system (25), activation of the hypothalamic-pituitary-adrenal axis with increased cortisol secretion (27), impairment of peripheral sensitivity to insulin (28), and increase of arteriolar tone (29), but none of these potential mechanisms has been conclusively demonstrated (30). It is known that the vascular endothelium generates many biologically active substances that contribute to the regulation of vascular tone (11) and, in the last decade, the study of alcohol-induced endothelial functional modifications has received much attention because the complex relationships between alcohol and blood pressure might result from opposite influences of different alcohol intakes on the vascular endothelium.…”

Study of Various Clinical Presentations, Laboratory Parameters and Echocardiographic Findings in Newly Diagnosed Hypertensive Patients

“…28 Association of alchohol and blood pressure is also explained by few studies. [29][30][31] Family history of CVD is important for hypertension because family members share genes, behaviors, lifestyles and environments that can influence their health and their risk for disease. 32 Dyslipidemia causes endothelial damage and loss of physiological vasomotor activity, this damage may manifest as elevated blood pressure.…”

A Conceptual Framework for Studying Alcohol Intake and Blood Pressure on Historically Black College and University Campuses

“…This is an indication that light to moderate (< 2 drinks per day for men and < 1 drink per day for women) consumption of beer, red wine, or white wine may have a somewhat protective effect related to hypertension (Sesso, Cook, Buring, Manson, & Gaziano, 2008). Chronic and heavy alcohol consumption may disturb red blood cell Na + (sodium) metabolism, contributing to increased vascular resistance leading to elevated blood pressure (Coca, Aguilera, De la Sierra, Sanchez, Picado, Lluch et al, 1992). This becomes more salient if the person consuming the alcohol is not also on a low sodium diet.…”