Hypertension and chronic ethanol consumption: What do we know after a century of study?

Abstract

The influences of life habits on the cardiovascular system may have important implications for public health, as cardiovascular diseases are among the leading causes of shorter life expectancy worldwide. A link between excessive ethyl alcohol (ethanol) consumption and arterial hypertension was first suggested early last century. Since then, this proposition has received considerable attention. Support for the concept of ethanol as a cause of hypertension derives from several epidemiologic studies demonstrating that in the general population, increased blood pressure is significantly correlated with ethanol consumption. Although the link between ethanol consumption and hypertension is well established, the mechanism through which ethanol increases blood pressure remains elusive. Possible mechanisms underlying ethanol-induced hypertension were proposed based on clinical and experimental observations. These mechanisms include an increase in sympathetic nervous system activity, stimulation of the renin-angiotensin-aldosterone system, an increase of intracellular Ca(2+) in vascular smooth muscle, increased oxidative stress and endothelial dysfunction. The present report reviews the relationship between ethanol intake and hypertension and highlights some mechanisms underlying this response. These issues are of interest for the public health, as ethanol consumption contributes to blood pressure elevation in the population.

Alcohol and cardiovascular diseases: where do we stand today?

“…Findings differed with respect to the presence of higher blood pressure amongst light-moderate drinkers compared to abstainers, with several studies showing lower pressures in lighter drinkers, especially amongst women [18][19][20][21][22]. Figure 1 presents these associations from a cross-sectional analysis by our group in 1977 of men and women of three racial groups [21].…”

“…In Asians, the alcohol-HTN association seems to be independent from alcohol-induced flushing, a phenomenon that is due to elevated blood acetaldehyde levels produced by a common genetic polymorphism in this racial group [18]. Heightened sympathetic nervous system responsiveness is widely considered to have a role in this relationship [18][19][20]. Sympathetic overactivity occurs during withdrawal from very heavy drinking, but was not seen in the above-mentioned studies [23][24][25][26][27].…”

“…Experimental data in humans and animals demonstrate no acute (minutes to hours) blood pressure rise after alcohol exposure [18][19][20]. Substantial mealtime drinking in the evening appears to depress pressure during the night for up to 8 h, followed by pressure increases the next morning [18].…”

“…As discussed in a recent review [20], solid evidence regarding the biological mechanisms of the alcohol-HTN association remains elusive. Data are inconsistent with respect to several potential neuroendocrine mechanisms [18][19][20].…”

Stem cell therapy in intracerebral hemorrhage rat model

“…As a matter of fact, it is estimated that about 50% of ICH cases are caused by chronic hypertension [1] . There is a well established liaison between regular consumption of alcoholic beverages and high blood pressure, being this effect independent of age, body mass, smoking habits and physical activity [16][17][18] . Hypertension and ICH incidence are also linked to other lifestyle-related risk factors, such as smoking [19,20] , physical inactivity [21] , and high dietary sodium and/or fat consumption [22,23] .…”