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Human hypertension is associated in a decrease in NO bioavailability and an increase in oxidative stress.[12] Decreased catalase and/or superoxide dismutase and reduced levels of reactive oxygen species (ROS) or reactive nitrogen species (RNS) scavengers such as glutathione, and vitamins C and E also contribute to oxidative stress.[13,14] Activation of reduction-oxidation (redox)-dependent signaling cascades and NADPH oxidase-driven generation of ROS are involved in the role of angiotensin-II-induced hypertension.[15] Angiotensin II stimulates nonphagocytic NADPH oxidase, causing the accumulation of hydrogen peroxide, superoxide, and peroxynitrite.[16] In obesity and diabetes that are usually associated with hypertension, chronic oxidative stress is present.[17,18,19,20] In this regard, caloric restriction in fasting and obese subjects leads to a marked reduction in ROS generation and other indices of oxidative stress.[17] A reduction in superoxide dismutase and glutathione peroxidase activity have been observed in newly diagnosed and untreated hypertensive subjects, which are inversely correlated with blood pressure

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