Nitric oxide in acute renal failure: NOS versus NOS

摘要: Nitric oxide in acute renal failure: NOS versus NOS. This overview provides information on the pathophysiology of inducible nitric synthase/nitric (iNOS/NO) system injury to cultured tubular epithelia, freshly isolated proximal tubules, and whole organ after hypoxic or ischemic insult. The findings emphasize role concomitant oxidative nitrosative stress peroxynitrite ensuing dysfunction. Scavenging using seleno-organic compounds like ebselen renoprotection against injury. These sequelae ischemia are a result endothelial dysfunction, which is most probably responsible for "no-reflow" phenomenon further aggravation during early reperfusion period. Recent studies have demonstrated that transplantation functional cells into kidney provided dramatic renoprotective effect. In conclusion, intricate relations between epithelial cells, based part synthases, perturbed primarily as dysfunction precipitating