NO bioavailability, endothelial dysfunction, and acute renal failure: new insights into pathophysiology.
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.
Goligorsky
Michael S
MS
Department of Medicine, New York Medical College, Valhalla 10595, USA. michael_goligorsky@nymc.edu
Brodsky
Sergey V
SV
Noiri
Eisei
E
D058186:Acute Kidney Injury / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology*; D001682:Biological Availability; D004730:Endothelium, Vascular / Q000201:enzymology / Q000503:physiopathology; D006801:Humans; D007677:Kidney Function Tests; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D011379:Prognosis; D018570:Risk Assessment; D012720:Severity of Illness Index
C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III