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The decrease in NO will also lead to reduced acetylcholine-mediated vasodilation, and an overall increase in ROS is associated in the reduction in the bioavailability of NO.[37] Urotensin-II which is the most potent identified vasoconstrictor also acts through the activation of NADPH oxidase.[31] In addition, overexpression of inducible NOS increases blood pressure via central activation of the sympathetic nervous system, which is mediated by an increase in oxidative stress.[38] In general, although there are multiple sources producing ROS, the most potential sources of excessive ROS in hypertension are as follows: NADPH oxidase, eNOS, mitochondria, xanthine oxidase, cytochrome P450 epoxygenase, cycloxygenase 1 and 2, transition metals (e.g
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