ABSTRACT:
Reactive oxygen species are oxygen derivative which influence many physiological processes. In normal physiological conditions, ROS are produced in a controlled manner at low concentrations and function as signaling molecules regulating vascular contraction-relaxation and cell growth. Increased ROS bioavailability and altered redox signaling (oxidative stress) have been implicated in chronic diseases including hypertension i.e. imbalance between superoxide and nitric oxide production leading to reduced vasodilation, resulting in development of hypertension. Hypertension caused by angiotensin II is dependent on vascular superoxide (O2-) production. The nicotinamide adenine dinucleotide phosphate (NAD[P]H) oxidase is a major source of vascular O2- and is activated by angiotensin II in- vitro. Activation of oxidative stress may result in vascular injury and in the progression of atherosclerosis. All these effects on the vasculature may explain how increased oxidative stress can cause hypertension.
