Roles of oxidative stress and antioxidant therapy in chronic kidney disease and hypertension

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Abstract
Oxidative stress is frequently associated with, and is partly involved in, the pathogenesis of chronic renal failure, hypertension and their complications. In the past few years, considerable progress has been made in deciphering the impact and the molecular mechanism of oxidative stress in these disorders. This article is intended to provide an overview of oxidative stress in hypertension and chronic renal failure. Recent studies have provided irrefutable evidence that oxidative stress can cause hypertension and hypertension can cause oxidative stress. The upregulation of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase and the tubulointerstitial accumulation of activated T cells, macrophages and superoxide-producing cells are partly responsible for oxidative stress in several models of hypertension. Antioxidant therapy alleviates hypertension, averts nuclear factor kappa B activation, and mitigates tubulointerstitial inflammation in hypertensive animals. Oxidative stress contributes to hypertension, endothelial dysfunction and brain disorders in chronic renal failure animals, and is partly caused by the upregulation of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase and the downregulation of superoxide dismutase. Oxidative stress, hypertension and inflammation are closely interrelated and involve a spiralling vicious cycle that can lead to progressive deterioration of hypertension and target organ damage.