Bradykinin stimulates prostaglandin E2production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosain vitro

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Abstract

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.

Summary

Objectives:To: 1) characterise and quantify PGE2 outputinvitro; 2) examine the sensitivity of PGE2 production to exogenous bradykinin (BK) exposure; 3) determine the contribution of the COX-1 and COX-2 pathways to basal and BK-stimulated PGE2 production; and 4) measure if BK influences electrogenic ion transport in equine gastric mucosaein vitro.

Summary

Methods:Full thickness gastric sheets were obtained from horses atpost 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.

Summary

Results:BK administration increased PGE2 output from the basolateral but not the apical faces of both tissue types. Piroxicam, but not NS-398, reduced basolateral PGE2 release below control levels in both tissue types. Both piroxicam and NS-398 pretreatment inhibited BK-stimulated PGE2 release. In separate experiments, BK was without effect upon electrophysiological parameters of tissues mounted in Ussing chambers.

Summary

Conclusions:PGE2 is produced by the nonglandular and glandular equine gastric mucosaein vitro. Significantly more PGE2 is released basolaterally than apically. BK stimulated the production of PGE2 from the basolateral side of both tissue types. These findings suggest that COX-1 is a significant pathway for basal PGE2 production from the basolateral faces of both nonglandular and glandular equine gastric mucosaein vitro.

Summary

Potential relevance:The identification of the cells responsible for basolateral PGE2 release, via both COX-1 and COX-2 pathways, under basal and BK-stimulated conditions requires further study.

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