The British Journal of Rheumatology, Vol 37, 246-257, Copyright © 1998 by British Society for Rheumatology
DO Stichtenoth and JC Frolich
Nitric oxide (NO) is synthesized from L-arginine by the NO synthases. At
present, mainly three NO synthase isoenzyme groups are differentiated: two
constitutive NO synthases, responsible for homeostatic cardiovascular and
neuronal functions of NO, and an inducible NO synthase. After induction by
certain cytokines or endotoxin, this latter isoform produces large
quantities of NO with cyto- and bacteriotoxic effects. High amounts of NO,
synthesized systemically and intra-articularly, play an important role in
inflammatory joint diseases, as shown in animal models of arthritis and in
patients with rheumatoid arthritis or spondyloarthropathies. In
experimental arthritis, administration of NO synthase inhibitors profoundly
reduced disease activity. In humans, beneficial effects of NO synthesis
inhibition are inferred from indirect evidence: glucocorticoids, inhibiting
induction of the inducible NO synthase, reduce enhanced NO synthesis and
disease activity. Thus, selective inhibition of the pathologically enhanced
NO synthesis emerges as a new experimental therapeutic approach in the
treatment of inflammatory joint diseases.
REVIEWS
Nitric oxide and inflammatory joint diseases
Department of Clinical Pharmacology, Hannover Medical School, Germany.
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