Bradykinin stimulates prostaglandin E2 production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosa in vitro.
Authors: Morrissey N K, Bellenger C R, Baird A W
Journal: Equine veterinary journal
Summary
# Editorial Summary Understanding how the equine stomach produces protective prostaglandins—particularly prostaglandin E2 (PGE2)—remains poorly characterised, yet this knowledge is crucial for interpreting how anti-inflammatory drugs and inflammatory mediators affect gastric health. Morrissey and colleagues used an in vitro model with full-thickness gastric tissue mounted in specialised chambers to quantify PGE2 production from both the nonglandular (squamous) and glandular regions of the stomach, examining how bradykinin (a potent inflammatory mediator released during tissue damage) influenced this response, and determining which cyclooxygenase (COX) pathways were responsible. Bradykinin significantly increased PGE2 release from the basolateral (blood-facing) surface of both tissue types, but not from the apical (luminal) surface, suggesting the protective response is directed toward the systemic circulation rather than the stomach contents. Importantly, whilst COX-2-selective inhibition only blocked the bradykinin-stimulated increase in PGE2, non-selective COX inhibitors reduced baseline PGE2 production below control levels, indicating that COX-1 is the primary enzyme maintaining protective basal prostaglandin levels in equine gastric mucosa. For practitioners, these findings support judicious use of non-selective NSAIDs in horses predisposed to gastric disease and suggest that COX-1-sparing strategies may better preserve the stomach's intrinsic cytoprotective mechanisms, particularly in inflammatory conditions where bradykinin levels are elevated.
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Practical Takeaways
- •Understanding COX-1 versus COX-2 contributions to gastric PGE2 production may inform selection of non-steroidal anti-inflammatory drugs (NSAIDs) for horses requiring gastric protection
- •The directional (basolateral) preference for PGE2 release suggests mucosal protection mechanisms are primarily targeted toward the underlying tissue rather than the luminal surface
- •Bradykinin's role in stimulating protective prostaglandins indicates inflammatory mediators may trigger compensatory cytoprotective responses in equine gastric mucosa
Key Findings
- •Bradykinin stimulates prostaglandin E2 (PGE2) production from the basolateral side of both nonglandular and glandular equine gastric mucosae in vitro
- •Significantly more PGE2 is released basolaterally than apically from equine gastric tissues
- •COX-1 is identified as a significant pathway for basal PGE2 production, while both COX-1 and COX-2 contribute to bradykinin-stimulated PGE2 release
- •Bradykinin administration had no effect on electrophysiological parameters or ion transport in equine gastric mucosae