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Influence on intestinal secretion of eicosanoids.
J Rask-Madsen1, K Bukhave, E Beubler
1Department of Medicine G, Bispebjerg Hospital, University of Copenhagen, Denmark.
Journal of Internal Medicine. Supplement
|January 1, 1990
Summary
Cholera toxin stimulates 5-hydroxytryptamine (5-HT) release, leading to prostaglandin E2 (PGE2) production. This pathway contributes to intestinal secretion independently of cyclic AMP (cAMP).
Area of Science:
- Gastroenterology
- Molecular Biology
- Pharmacology
Background:
- Eicosanoids modulate intestinal secretion.
- Cyclic adenosine monophosphate (cAMP) is a known cholera mediator.
- 5-hydroxytryptamine (5-HT) and prostaglandin E2 (PGE2) roles in cholera are emerging.
Purpose of the Study:
- Investigate the roles of 5-HT and PGE2 in cholera toxin (CT)-induced intestinal secretion.
- Determine the relationship between CT, 5-HT, PGE2, and cAMP in intestinal fluid secretion.
Main Methods:
- In vivo studies in rat jejunum.
- In vitro secretion assays.
- Measurement of 5-HT, PGE2, and cAMP levels.
- Pharmacological inhibition using indomethacin and ketanserin.
Main Results:
- CT increased 5-HT and PGE2 release in rat jejunum.
- 5-HT induced secretion with increased PGE2 but unchanged cAMP.
- Indomethacin and ketanserin reduced CT-induced PGE2 release and fluid secretion.
- Vasoactive intestinal polypeptide (VIP)-induced secretion involved cAMP, not PGE2, and was unaffected by inhibitors.
Conclusions:
- CT stimulates 5-HT release, which triggers PGE2 release.
- PGE2 contributes to intestinal secretion via a local intramural reflex.
- This CT-induced secretion mechanism is independent of cAMP.