NO bioavailability, endothelial dysfunction, and acute renal failure: New insights into pathophysiology

被引:69
作者
Goligorsky, MS
Brodsky, SV
Noiri, E
机构
[1] New York Med Coll, Div Nephrol, Dept Med, Valhalla, NY 10595 USA
[2] New York Med Coll, Dept Pharmacol, Valhalla, NY 10595 USA
[3] Univ Tokyo, Dept Med, Tokyo, Japan
关键词
D O I
10.1016/j.semnephrol.2004.04.003
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
This brief overview sketches current evidence of imbalance between inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS), role of oxidant stress, and generation of peroxynitrite in the pathophysiology of acute ischemic renal injury. The development of endothelial cell dysfunction at early stages of experimental acute renal ischemia is the focus of the review, with the results of recent studies on amelioration of renal injury by the infused endothelial cells engrafting in the renal microcirculation. Finally, this article provides some future perspectives on the potential usefulness of endothelial progenitor cells in the prevention and treatment of acute renal failure. © 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:316 / 323
页数:8
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