Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2004 Jul;24(4):354-65.
doi: 10.1016/j.semnephrol.2004.04.007.

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

Paul S Modlinger  1 , Christopher S Wilcox, Shakil Aslam
Affiliations
Review

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

Paul S Modlinger et al. Semin Nephrol. 2004 Jul.

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 with CRF show decreased endothelium-dependent vasodilatation to acetylcholine, have increased markers of oxidative stress, and diminished antioxidant activity. Therapy for oxidative stress has focused on antioxidants and agents that modify the renin-angiotensin system. The effects of such treatments are more compelling in animal models than in human studies.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types

LinkOut - more resources

-