Role of Nitric Oxide in Inflammatory ConditionsBlantz R.C. · Munger K.
University of California, San Diego, Calif., and Veterans Administration San Diego Healthcare System, San Diego, Calif., USA
Nitric oxide (NO) plays an important regulatory/modulatory role in a variety of inflammatory conditions. NO is a small, short-lived molecule that is released from a variety of cells in response to homeostatic and pathologic stimuli. It may act as a vasodilator and a platelet inhibitor and may interfere with adhesion molecules to prevent neutrophil adhesion. NO release may also lead to the formation of highly reactive species such as peroxynitrite and stable nitrosothiols and may cause mitochondrial damage and nitration of protein tyrosine residues. In addition, NO inhibits cell proliferation via inhibition of polyamine synthesis and cell uptake and may well act as a ‘brake’ on the proliferative response following cytokine exposure. All three isoforms of nitric oxide synthases are found in the kidney during inflammation. The site of NO release impacts significantly on its net function and structural impact. NO plays a protective role in many forms of immune injury, such as nephrotoxic serum-induced glomerulonephritis, autoimmune tubular interstitital nephritis, and experimental allergic encephalomyelitis. NO overproduction in sepsis, after cytokine exposure, inducible NO synthase transcription, and local inflammation can autoinhibit endothelial NO synthase, leading to selective renal and mesenteric vasoconstriction.
© 2002 S. Karger AG, Basel
Roland C. Blantz, MD
VASD Healthcare System
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San Diego, CA 92161 (USA)
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Number of Print Pages : 6
Number of Figures : 0, Number of Tables : 1, Number of References : 54
Founded 1964 by G. Richet and G.E. Schreiner
Vol. 90, No. 4, Year 2002 (Cover Date: April 2002)
Journal Editor: G.M. Berlyne, Brooklyn, N.Y./Beersheva; S. Ito, Sendai
ISSN: 0028–2766 (print), 1423–0186 (Online)
For additional information: http://www.karger.com/journals/nef