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
Relevant Article
- 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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