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Vol. 90, No. 4, 2002
Issue release date: April 2002
Section title: Distinguished Scientists Lecture Series. Section Editors: J.C.M. Chan; R.J. Krieg, Jr.; J.I. Scheinmann (Richmond, Va.)
Nephron 2002;90:373–378
(DOI:10.1159/000054723)

Role of Nitric Oxide in Inflammatory Conditions

Blantz R.C. · Munger K.
University of California, San Diego, Calif., and Veterans Administration San Diego Healthcare System, San Diego, Calif., USA

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Article / Publication Details

First-Page Preview
Abstract of Distinguished Scientists Lecture Series. Section Editors: J.C.M. Chan; R.J. Krieg, Jr.; J.I. Scheinmann (Richmond, Va.)

Published online: 4/8/2002
Issue release date: April 2002

Number of Print Pages: 6
Number of Figures: 0
Number of Tables: 1

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

For additional information: http://www.karger.com/NEF

Abstract

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


  

Author Contacts

Roland C. Blantz, MD
VASD Healthcare System
3350 La Jolla Village Drive
San Diego, CA 92161 (USA)
Tel. +1 858 552 7528, Fax +1 858 552 7549, E-Mail rblantz@ucsd.edu

  

Article Information

Number of Print Pages : 6
Number of Figures : 0, Number of Tables : 1, Number of References : 54

  

Publication Details

Nephron
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


Article / Publication Details

First-Page Preview
Abstract of Distinguished Scientists Lecture Series. Section Editors: J.C.M. Chan; R.J. Krieg, Jr.; J.I. Scheinmann (Richmond, Va.)

Published online: 4/8/2002
Issue release date: April 2002

Number of Print Pages: 6
Number of Figures: 0
Number of Tables: 1

ISSN: 1660-8151 (Print)
eISSN: 2235-3186 (Online)

For additional information: http://www.karger.com/NEF


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