Nitric oxide in acute renal failure: NOS versus NOS

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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat

Published on: July 3, 2013

Michael S Goligorsky1, Sergey V Brodsky, Eisei Noiri

  • 1Department of Medicine, State University of New York, Stony Brook, NY 11794-8152, USA. mgoligorsky@mail.som.sunysb.edu

Kidney International
|February 19, 2002
PubMed

Insights

Renal ischemia causes injury via inducible nitric oxide synthase/nitric oxide (iNOS/NO) pathways, leading to oxidative stress and peroxynitrite formation. Seleno-organic compounds and endothelial cell transplantation offer renoprotection against this kidney damage.

Area of Science:

  • Nephrology
  • Pathophysiology
  • Biochemistry

Background:

  • The inducible nitric oxide synthase/nitric oxide (iNOS/NO) system plays a critical role in renal tubular injury following hypoxic or ischemic insults.
  • Oxidative and nitrosative stress, mediated by peroxynitrite, are key contributors to renal dysfunction after ischemia.

Purpose of the Study:

  • To provide an overview of the pathophysiology of iNOS/NO system in renal injury.
  • To highlight the role of peroxynitrite in renal dysfunction and explore renoprotective strategies.
  • To elucidate the interplay between endothelial and epithelial cells in renal ischemia.

Main Methods:

  • Review of existing literature on iNOS/NO system in cultured renal tubular epithelia, isolated proximal tubules, and whole organs.
  • Analysis of the impact of hypoxic or ischemic insult on renal pathophysiology.
  • Evaluation of renoprotective effects of peroxynitrite scavengers and endothelial cell transplantation.

Main Results:

  • Concomitant oxidative and nitrosative stress, with peroxynitrite formation, significantly contributes to renal dysfunction post-ischemia.
  • Seleno-organic compounds, such as ebselen, demonstrate renoprotective effects by scavenging peroxynitrite.
  • Endothelial dysfunction is implicated in the 'no-reflow' phenomenon and exacerbates tubular ischemia during reperfusion, with endothelial cell transplantation showing renoprotective benefits.

Conclusions:

  • The pathophysiology of renal ischemia involves complex interactions between endothelial and epithelial cells, significantly influenced by endothelial dysfunction.
  • Perturbations in the iNOS/NO system, particularly endothelial dysfunction, precipitate epithelial injury and contribute to overall renal damage.
  • Targeting peroxynitrite and enhancing endothelial function represent promising therapeutic avenues for renoprotection against ischemic injury.

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