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Crucial role for 5-HT in cholera toxin but notEscherichia coliheat-labile enterotoxin-intestinal secretion in rats

Authors
Journal
Gastroenterology
0016-5085
Publisher
Elsevier
Publication Date
Volume
115
Issue
4
Identifiers
DOI: 10.1016/s0016-5085(98)70260-4
Disciplines
  • Biology
  • Medicine
  • Pharmacology

Abstract

Abstract Background & Aims: Many consider cholera toxin (CT) and Escherichia coli heat-labile enterotoxin (LT) to be functionally identical. Both increase intracellular adenosine 3',5'-cyclic monophosphate concentration; however, differences between the two and the severity of the diseases they cause have been reported. The secretagogue 5-hydroxytryptamine (5-HT) is implicated in CT-induced secretion, but its role in LT-induced secretion is unclear. We tested the hypothesis that LT fails to recruit 5-HT in its secretory processes. Methods: In vivo small intestinal perfusions were undertaken in adult male Wistar rats after incubation with equipotent doses of CT or LT, or saline. Small intestinal 5-HT release and the effect on net small intestinal water and electrolyte transport of (1) pharmacological depletion of 5-HT; (2) blockade of 5-HT type 2, 3, and 4 receptors; and (3) pretreatment with lidocaine, hexamethonium, and atropine were determined. Results: CT- but not LT-induced secretion was accompanied by 5-HT release, reduced by 5-HT depletion, and inhibited by each 5-HT antagonist. By contrast, lidocaine and hexamethonium inhibited secretion induced by both toxins. Conclusions: LT induces secretion without recruiting a 5-HT–dependent cascade. This may account for differences in clinical severity of the diseases CT and LT cause and has implications for the development of antisecretory therapies. GASTROENTEROLOGY 1998;115:883-890

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