Alcohol and Hypertension-A Fresh Look on the Mechanistic Aspects of a Fatal Epidemiologic Relationship.

Abstract

Arterial hypertension is a key trigger for all major, life-threatening cardiovascular events such as arrhythmia, stroke, cardiac infarction and heart failure. Ethanol consumption has been identified as a critical risk factor, which promotes hypertension and thereby corrupts cardiovascular health and limits overall life expectancy. For heavy drinkers (≥72 g/day), reduction in half of the alcohol consumption reportedly results in considerable decreases in systolic and diastolic blood pressure levels amounting to 5.50 and 3.97 mmHg, respectively. Based on the complex network of ethanol effects on mammalian physiology, diverse mechanistic concepts have been postulated for a causal linkage between alcohol consumption and distorted blood pressure regulation. The impact of ethanol on the cardiovascular system involves a wide range of ethanol-sensitive cell types, ranging from neurons to vascular smooth muscle, endothelial and immune-cells, all of which express an interdependent array of potential ethanol target structures. Here, we provide an update on currently available evidence for a causal link between alcohol consumption and the etiology of arterial hypertension. The potential role of ethanol target structures with particular focus on membrane ion channels is discussed along with novel concepts of lipid-dependent modulation of signaling processes in the plasma membrane by ethanol.