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Verapanzil inhibits in‐vitro leucotriene B4 release by rectal mucosa in active ulcerative colitis
Author(s) -
GERTNER D. J.,
RAMPTON D. S.,
STEVENS T. R. J.,
LENNARDJONES J. E.
Publication year - 1992
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.1992.tb00259.x
Subject(s) - verapamil , ulcerative colitis , medicine , leukotriene b4 , eicosanoid , colitis , calcium , intestinal mucosa , pharmacology , calcium channel , gastroenterology , prostaglandin e2 , antagonist , nifedipine , endocrinology , inflammation , arachidonic acid , chemistry , biochemistry , enzyme , receptor , disease
SUMMARY Increased mucosal eicosanoid synthesis occurs in active ulcerative colitis; suppression of the synthesis of pro‐inflammatory leucotrienes could be therapeutically useful. Neutrophil 5‐lipoxygenase is calcium‐dependent. In this study, the effect of the calcium channel antagonist, verapamil, on the release of eicosanoids by colitic rectal mucosal biopsies has been examined. Verapamil in therapeutic concentration (5 μ g/ml, 10 ‐5 M) reduced leucotriene B4 release from actively inflamed rectal mucosa by 30% (from 60 (5.0 S.E.M.) ng/g wet weight/20 min without, to 42 (5.7 S.E.M.) with verapamil, P < 0.05), but had no effect on leucotriene B4 release by rectal biopsies taken from patients with quiescent ulcerative colitis (39 (2.8 S.E.M.) ng/g wet weight/20 min without, and 43 (5.0 S.E.M.) with verapamil). Verapamil did not affect mucosal prostaglandin E 2 release. The results suggest that, in active ulcerative colitis, verapamil inhibits mucosal 5‐lipoxygenase activity and warrants therapeutic evaluation.