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Gut 1998;42:152-153; doi:10.1136/gut.42.2.152
Copyright © 1998 BMJ Publishing Group Ltd & British Society of Gastroenterology.
GUT 1998;42:152-153 ( February )

COMMENTARY

See article on page 180

NOS inhibitors in colitis: a suitable case for treatment?

The first 150 words of the full text of this article appear below.

Nitric oxide (NO) is now well characterised as a physiologically important molecule, acting most notably as an intra- and intercellular messenger within the cardiovascular and nervous systems.1 To fulfil these functions NO is produced in a tightly controlled manner by calcium dependent, constitutively expressed nitric oxide synthases (cNOS) present within endothelial and neural cells. Under pathological conditions, however, NO acts very differently from a benign signalling molecule. In these circumstances NO is produced in large, apparently tissue damaging amounts by inducible, calcium unregulated nitric oxide synthases (iNOS). For example, in inflammatory bowel disease the presence of high local concentrations of pro-inflammatory cytokines, such as interleukin 8, is associated with the induction of iNOS and so the continuous local generation of NO,2 3 possibly in very great amounts.4 Notably, this difference in NO production between cNOS and iNOS enzymes is not due, as is often remarked, to the inducible isoform of NO synthase . . . [Full text of this article]


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Increased expression of an inducible isoform of nitric oxide synthase and the formation of peroxynitrite in colonic mucosa of patients with active ulcerative colitis
H Kimura, R Hokari, S Miura, T Shigematsu, M Hirokawa, Y Akiba, I Kurose, H Higuchi, H Fujimori, Y Tsuzuki, H Serizawa, and H Ishii
Gut 1998 42: 180-187. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

  • ZHANG, Z, NAUGHTON, D P, CARTY, E, RAMPTON, D S (1999). Excess nitric oxide in ulcerative colitis may be generated by nitric oxide synthase independent pathways. Gut 44: 439c-439 [Full Text]  

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