The observation that the excessive consumption of ethyl alcohol (ethanol) is associated with high blood
pressure is nearing its centennial mark. Mechanisms linking ethanol consumption and hypertension are complex and not
fully understood. It is established that chronic ethanol consumption leads to hypertension and that this process is a multimediated
event involving increased sympathetic activity, stimulation of the renin-angiotensin-aldosterone system with a
subsequent increase in vascular oxidative stress and endothelial dysfunction. Under physiological conditions, reactive
oxygen species (ROS) play an important role as a signaling molecule in the control of vascular tone and endothelial
function. Increased ROS bioavailability is associated with important processes underlying vascular injury in
cardiovascular disease such as endothelial dysfunction, vascular remodeling, and inflammation. Studies focusing on
molecular mechanisms showed a link between overproduction of ROS in the vasculature and ethanol-induced
hypertension. Of the ROS generated in vascular cells, superoxide anion (O2−) and hydrogen peroxide (H2O2) appear to be
especially important. Ethanol-mediated generation of O2− and H2O2 in vascular tissues is associated with elevations in
intracellular calcium ([Ca2+]i), reduced nitric oxide (NO) bioavailability, endothelial dysfunction and vasoconstriction.
O2− can also act as a vascular signaling molecule regulating signaling pathways that lead to vascular contraction. Thus,
through increased generation of ROS and activation of redox-sensitive pathways, ethanol induces vascular dysfunction, a
response that might contribute to the hypertension associated with ethanol consumption. The present article reviews the
role of ROS in vascular (patho)biology of ethanol.
Keywords: Endothelial dysfunction, ethanol, hypertension, oxidative stress, reactive oxygen species, superoxide anion.
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