The cellular metabolism of oxygen generates potentially deleterious reactive oxygen species, including superoxide anion, hydrogen peroxide and hydroxyl radical. Under normal physiologic conditions, the rate and magnitude of oxidant formation is balanced by the rate of oxidant elimination. However, an imbalance between pro-oxidants and antioxidants results in oxidative stress, which is the pathogenic outcome of the overproduction of oxidants that overwhelms the cellular antioxidant capacity. There is growing evidence that increased oxidative stress and associated oxidative damage are mediators of vascular injury in cardiovascular pathologies, including hypertension, atherosclerosis and ischemia-reperfusion. This development has evoked considerable interest because of the possibilities that therapies targeted against reactive oxygen intermediates by decreasing the generation of reactive oxygen species and/or by increasing availability of antioxidants may be useful in minimizing vascular injury. This review focuses on the vascular actions of reactive oxygen species, the role of oxidative stress in vascular damage in hypertension and the therapeutic potential of modulating oxygen radical bioavailability in hypertension. In particular, the following topics will be highlighted: chemistry and sources of reactive oxygen species, antioxidant defense mechanisms, signaling events mediated by reactive oxygen species, role of reactive oxygen species in hypertension and the putative therapeutic role of antioxidants in cardiovascular disease.