Premium
Bradykinin stimulates prostaglandin E 2 production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosa in vitro
Author(s) -
MORRISSEY N. K.,
BELLENGER C. R.,
BAIRD A. W.
Publication year - 2008
Publication title -
equine veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.82
H-Index - 87
eISSN - 2042-3306
pISSN - 0425-1644
DOI - 10.2746/042516408x293556
Subject(s) - bradykinin , piroxicam , cyclooxygenase , prostaglandin e , ussing chamber , prostaglandin e2 , chemistry , in vitro , prostaglandin , medicine , endocrinology , gastric mucosa , histamine , pharmacology , biochemistry , biology , stomach , receptor , enzyme , pathology , alternative medicine
Summary Reasons for performing study : There are few data available regarding regulation of prostaglandin (PG) generation by equine gastric mucosae and the role of the cyclooxygenase (COX) isoforms in their production. Objectives : To: 1) characterise and quantify PGE 2 output in vitro ; 2 ) examine the sensitivity of PGE 2 production to exogenous bradykinin (BK) exposure; 3) determine the contribution of the COX‐1 and COX‐2 pathways to basal and BK‐stimulated PGE 2 production; and 4) measure if BK influences electrogenic ion transport in equine gastric mucosae in vitro.Methods : Full thickness gastric sheets were obtained from horses at post mortem , stripped of muscle layers and mounted in Ussing chambers. Tissues were exposed to bradykinin (BK, 0.1 μmol/l) either alone, or following pretreatment with a selective COX‐2 inhibitor (NS‐398, 1 μmol/l) or a nonselective COX inhibitor (piroxicam, 1 μmol/l), or were untreated. Results : BK administration increased PGE 2 output from the basolateral but not the apical faces of both tissue types. Piroxicam, but not NS‐398, reduced basolateral PGE 2 release below control levels in both tissue types. Both piroxicam and NS‐398 pretreatment inhibited BK‐stimulated PGE 2 release. In separate experiments, BK was without effect upon electrophysiological parameters of tissues mounted in Ussing chambers. Conclusions : PGE 2 is produced by the nonglandular and glandular equine gastric mucosae in vitro. Significantly more PGE 2 is released basolaterally than apically. BK stimulated the production of PGE 2 from the basolateral side of both tissue types. These findings suggest that COX‐1 is a significant pathway for basal PGE 2 production from the basolateral faces of both nonglandular and glandular equine gastric mucosae in vitro.Potential relevance : The identification of the cells responsible for basolateral PGE 2 release, via both COX‐1 and COX‐2 pathways, under basal and BK‐stimulated conditions requires further study.