1. The molecular sources of reactive oxygen species in hypertension.
- Author
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Puddu P, Puddu GM, Cravero E, Rosati M, and Muscari A
- Subjects
- Animals, Cytochrome P-450 Enzyme System physiology, Humans, Mitochondria metabolism, NADPH Oxidases physiology, Nitric Oxide Synthase Type III physiology, Oxidative Stress, Xanthine Dehydrogenase physiology, Hypertension metabolism, Reactive Oxygen Species metabolism
- Abstract
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.
- Published
- 2008
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