Oxidative stress and nitric oxide deficiency in the kidney: a critical link to hypertension?

There is growing evidence that oxidative stress contributes to hypertension. Oxidative stress can precede development of hypertension. In almost all models of hypertension, there is stress that, if corrected, lowers BP, whereas creation of oxidative stress normal animals can cause hypertension. There is overexpression of the p22(phox) Nox-1 components of NADPH oxidase and reduced expression of extracellular dismutase (EC-SOD) in the kidneys of ANG II-infused rodents, there is overexpression of p47(phox) and gp91(phox) and reduced expression of SOD with salt loading. Several mechanisms have been identified that make oxidative stress self-sustaining. Reactive oxygen species (ROS) can afferent arteriolar tone and reactivity both indirectly via potentiation of feedback and directly by microvascular mechanisms that diminish endothelium-derived relaxation factor/nitric oxide responses, generate a cyclo-oxygenase-2-dependent endothelial-derived contracting factor that activates thromboxane-prostanoid receptors, and enhance vascular smooth muscle cells reactivity. can diminish the efficiency with which the kidney uses O-2 for Na+ transport thereby diminish the Po-2 within the kidney cortex. This may place a break on ROS generation yet could further enhance vasculopathy and hypertension. There is a tight relationship between oxidative stress in the kidney and the development and the maintenance of hypertension.