“…Other potential mechanisms by which ethanol causes cardiovascular changes include increased ROS, reduced antioxidant defense, apoptotic cell death, mitochondrial stress, abnormalities in fatty acid metabolism and transport, and accelerated protein catabolism (10,36). In the cardiovascular system, specifically, ethanol consumption increases oxidative stress, decreases nitric oxide (NO) bioavailability, stimulates the renin-angiotensin-aldosterone system (RAAS), increases sympathetic nervous system activity, causes insulin resistance, stimulates the hypothalamic-pituitary axis (HPA) with cortisol excess, alters Ca 2 þ -Mg 2 þ handling, and stimulates the endothelin-1 system (10,(37)(38)(39)(40)(41)(42). These processes may individually and synergistically contribute to cardiovascular remodeling and dysfunction, myocardial and vascular oxidative/nitrosative stress, vascular hyperresponsiveness, endothelial dysfunction, and vascular inflammation observed with excessive ethanol consumption (10,38,(41)(42)(43).…”