期刊
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
卷 13, 期 1, 页码 93-99出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00041552-200401000-00013
关键词
antioxidants; atherosclerosis; hypertension; nicotinamide adenine; dinucleotide phosphate (reduced form) oxidase; oxidative stress; reactive oxygen intermediates; renal disease
Purpose of review 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 findings 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. Summary 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据