The molecular sources of reactive oxygen species in hypertension.
In both animal models and humans, increased blood pressure has been associated with oxidative stress in the vasculature, i.e. an excessive endothelial production of reactive oxygen species (ROS), which may be both a cause and an effect of hypertension. In addition to NADPH oxidase, the best characterized source of ROS, several other enzymes may contribute to ROS generation, including nitric oxide synthase, lipoxygenases, cyclo-oxygenases, xanthine oxidase and cytochrome P450 enzymes. It has been suggested that also mitochondria could be considered a major source of ROS: in situations of metabolic perturbation, increased mitochondrial ROS generation might trigger endothelial dysfunction, possibly contributing to the development of hypertension. However, the use of antioxidants in the clinical setting induced only limited effects on human hypertension or cardiovascular endpoints. More clinical studies are needed to fully elucidate this so called "oxidative paradox" of hypertension.
Department of Internal Medicine, Aging and Nephrological Diseases, University of Bologna and S Orsola-Malpighi Hospital, Bologna, Italy.
Paolo
P
Puddu
Giovanni Maria
GM
Puddu
Eleonora
E
Cravero
Marzia
M
Rosati
Antonio
A
Muscari
D000818:Animals; D003577:Cytochrome P-450 Enzyme System / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism; D019255:NADPH Oxidases / Q000502:physiology; D052250:Nitric Oxide Synthase Type III / Q000502:physiology; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014968:Xanthine Dehydrogenase / Q000502:physiology
D017382:Reactive Oxygen Species; D003577:Cytochrome P-450 Enzyme System; D052250:Nitric Oxide Synthase Type III; D014968:Xanthine Dehydrogenase; D019255:NADPH Oxidases