Reactive oxygen species and vascular remodeling in hypertension: still alive

Reactive oxygen species (ROS) are reactive derivatives of O<sub>2</sub> metabolism, including superoxide anion, hydrogen peroxide, hydroxyl radical and nitric oxide. All types of vascular cells produce ROS, primarily via cell membrane-associated NAD(P)H oxidase. Cardiovascular diseases, such as hypertension, are associated with increased ROS formation (oxidative stress). Oxidative excess in the vasculature reduces levels of the vasodilator nitric oxide, causes tissue injury, promotes protein oxidation and DNA damage, and induces proinflammatory responses. ROS are also important intracellular signalling molecules that regulate vascular function by modulating vascular cell contraction/dilation, migration, growth/apoptosis, and extracellular matrix protein turnover, which contribute to vascular remodelling. Interventions to decrease ROS bioavailability regress remodelling and reduce blood pressure in experimental hypertension. Such strategies may have therapeutic potential in cardiovascular diseases