Nitric oxide, oxidative stress, and progression of chronic renal failure

Seminars in Nephrology
Paul S ModlingerShakil Aslam

Abstract

Cellular injury or organ dysfunction from oxidative stress occurs when reactive oxygen species (ROS) accumulate in excess of the host defense mechanisms. The deleterious effect of ROS occurs from 2 principal actions. First, ROS can inactivate mitochondrial enzymes, damage DNA, or lead to apoptosis or cellular hypertrophy. Second, nitric oxide (NO), which is a principal endothelial-derived relaxing factor, reacts with superoxide anion (O2-) to yield peroxynitrite (ONOO-), which is a powerful oxidant and nitrosating agent. The inactivation of NO by O2- creates NO deficiency. Oxidative stress can promote the production of vasoconstrictor molecules and primary salt retention by the kidney. Several hypertensive animal models showed increased activity of nicotine adenine dinucleotide phosphate (NADPH) oxidase, which is the chief source of O2- in the vessel wall and kidneys. NO regulates renal blood flow, tubuloglomerular feedback (TGF), and pressure natriuresis. Animal models of NO deficiency develop hypertension, proteinuria, and glomerulosclerosis. Evidence is presented that chronic renal failure (CRF) is a state of NO deficiency secondary to decreased kidney NO production and/or increased bioinactivation of NO by O2-. Patients wit...Continue Reading

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