Reactive oxygen species contribute to the development of hypertension by inducing vascular contraction, endothelial dysfunction, hypertrophic remodeling, and renal tissue damage.
Hypertension is associated with an elevation of reactive oxygen species (ROS) and frequently also with an impairment of endogenous antioxidant mechanisms. Experimental manipulation of the redox state in vivo shows that ROS can be a cause of hypertension. During the development of the disease, ROS are generated by endogenous sources, notably the NADPH oxidase enzyme family and uncoupled nitric oxide synthase, due to a mutual reinforcement between ROS and humoral factors. The ROS affect multiple tissues, either directly or through nitric oxide depletion. In the vasculature, they induce contraction and endothelial dysfunction. In blood vessels and myocardium, they cause hypertrophic remodeling. In the kidneys, ROS promote salt reabsorption, decrease glomerular filtration, and lead to tissue damage. Finally, they also increase efferent sympathetic activity from the central nervous system. Progress in our understanding of the mechanisms of ROS formation and their plethora of pathophysiologic effects is expected to lead from simple antioxidant therapy to specific antihypertensive treatments.
Bernard Lassègue (Wed,) conducted a review in Hypertension. Reactive oxygen species (ROS) was evaluated. Reactive oxygen species contribute to the development of hypertension by inducing vascular contraction, endothelial dysfunction, hypertrophic remodeling, and renal tissue damage.