Oxidative stress and vascular damage in hypertension.
Metabolism of oxygen by cells generates potentially deleterious reactive oxygen species, including superoxide anion radical, 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 prooxidants and antioxidants results in oxidative stress, which is the pathogenic outcome of the overproduction of oxidants that overwhelms the cellular antioxidant capacity. There is increasing evidence that an elevation of oxidative stress and associated oxidative damages are mediators of vascular injury in various cardiovascular pathologies, including hypertension, atherosclerosis, and ischemia-reperfusion. This review focuses on the vascular effects of reactive oxygen species and the role of oxidative stress in vascular damage in hypertension.
Touyz
R M
RM
MRC Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, 110 Pine Avenue West, Montreal, Quebec H2W 1R7, Canada. touyzr@ircm.qc.ca
D000804:Angiotensin II / Q000378:metabolism; D004730:Endothelium, Vascular / Q000473:pathology; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism
D005609:Free Radicals; D000804:Angiotensin II; D013482:Superoxide Dismutase