Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ogawa, D.
Right arrow Articles by Makino, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ogawa, D.
Right arrow Articles by Makino, H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2002) 17: 2117-2121
© 2002 European Renal Association-European Dialysis and Transplant Association

Protective effect of a novel and selective inhibitor of inducible nitric oxide synthase on experimental crescentic glomerulonephritis in WKY rats

Daisuke Ogawa1, Kenichi Shikata1,, Mitsuhiro Matsuda1, Shinichi Okada1, Hitomi Usui1, Jun Wada1, Naoyuki Taniguchi2 and Hirofumi Makino1

1 Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, Shikata-cho, Okayama and 2 Department of Biochemistry, Osaka University Graduate School of Medicine, Yamadaoka, Suita, Osaka, Japan

Background. Nitric oxide (NO) plays important roles in a variety of pathophysiological processes. It has been reported that inducible NO synthase (iNOS) is upregulated in the glomeruli of patients with glomerulonephritis, although there has been no direct evidence that NO generated by iNOS contributes to the progression of glomerulonephritis. ONO-1714, a novel cyclic amidine analog, is a selective inhibitor of iNOS. To elucidate the role of iNOS in the pathogenesis of experimental crescentic glomerulonephritis, we examined the effect of ONO-1714 given to rats with nephrotoxic serum (NTS) nephritis.

Methods. We induced NTS nephritis in Wistar–Kyoto (WKY) rats. These rats were given ONO-1714 or physiological saline intraperitoneally for 14 days using an osmotic pump after intraperitoneal injection with NTS.

Results. Glomerular expression of iNOS and urinary excretion of NO metabolites (nitrite/nitrate) were increased in rats after injection of NTS. As compared with the control group, ONO-1714 significantly reduced proteinuria, crescent formation, glomerular infiltration of macrophages and urinary excretion of nitrite/nitrate.

Conclusion. The present results suggest that NO radicals generated by iNOS contribute to the progression of experimental crescentic glomerulonephritis in WKY rats. The selective iNOS inhibitor ONO-1714 may be beneficial for the treatment of crescentic glomerulonephritis.

Keywords: crescent; glomerulonephritis; inducible nitric oxide synthase; macrophage; nitric oxide; ONO-1714

Correspondence and offprint requests to: Kenichi Shikata, MD, PhD, Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.Email: shikata{at}md.okayama-u.ac.jp


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Am. Soc. Nephrol.Home page
L.-Q. Qiu, R. Sinniah, and S. I-H. Hsu
Coupled Induction of iNOS and p53 Upregulation in Renal Resident Cells May Be Linked with Apoptotic Activity in the Pathogenesis of Progressive IgA Nephropathy
J. Am. Soc. Nephrol., August 1, 2004; 15(8): 2066 - 2078.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.