Duality of nitric oxide in acute renal injury.

This brief overview focuses on the complexity of the distribution of nitric oxide (NO) synthases in the kidney and their regulation following acute renal injury. The authors attempt to provide clearcut distinctions between various targets of NO, describe its cytotoxic and renoprotective effects, and emphasize the role of combined oxidative and nitrozative stress in mediating renal injury. Furthermore, some strategies to pharmacologically manipulate the expression of NO synthases are described. This treatment of the subject is based on the authors' hypothesis that imbalance between the expression and activity of the inducible and constitutive endothelial isoforms of the enzyme is an important contributor to the pathophysiology of acute renal failure.