Renal endothelial dysfunction and impaired autoregulation after ischemia-reperfusion injury result from excess nitric oxide

Endothelial dysfunction in ischemic acute renal failure (IARF) has been attributed to both direct endothelial injury and to altered endothelial nitric oxide synthase (eNOS) activity, with either maximal upregulation of eNOS or inhibition of eNOS by excess nitric oxide (NO) derived from iNOS. We inve...

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Veröffentlicht in:	American journal of physiology. Renal physiology 2006-09, Vol.291 (3), p.F619-F628
Hauptverfasser:	Guan, Zhengrong, Gobé, Glenda, Willgoss, Desley, Endre, Zoltán H
Format:	Artikel
Sprache:	eng
Schlagworte:	Acute Kidney Injury - physiopathology Angiotensin II - pharmacology Animals Endothelium - physiopathology Homeostasis - drug effects Homeostasis - physiology In Vitro Techniques Indomethacin - pharmacology Kidney - physiopathology Methacholine Chloride - pharmacology NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - pharmacology Nitric Oxide - physiology Nitric Oxide Synthase Type II - antagonists & inhibitors Phenylephrine - pharmacology Rats Rats, Sprague-Dawley Reperfusion Injury - chemically induced Reperfusion Injury - physiopathology Vasoconstriction - drug effects
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