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5-HT2 and 5-HT3 receptor subtypes mediate cholera toxin-induced intestinal fluid secretion in the rat.

E Beubler1, G Horina

  • 1Department of Experimental and Clinical Pharmacology, Karl-Franzens-University, Graz, Austria.

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|July 1, 1990
PubMed
Summary
This summary is machine-generated.

Cholera toxin causes diarrhea by releasing 5-hydroxytryptamine (5-HT). Blocking both 5-HT2 and 5-HT3 receptors completely stops cholera toxin-induced fluid secretion in rats.

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Area of Science:

  • Gastroenterology
  • Pharmacology
  • Molecular Biology

Background:

  • Diarrhea in Asiatic cholera involves cyclic adenosine monophosphate, 5-hydroxytryptamine (5-HT), prostaglandins, and neuronal structures.
  • The precise role of 5-HT in mediating cholera secretion requires further elucidation.

Purpose of the Study:

  • To investigate the action of 5-HT in cholera secretion using in vivo rat jejunum models.
  • To determine the effects of 5-HT2 and 5-HT3 receptor antagonists on cholera toxin-induced fluid secretion.

Main Methods:

  • In vivo experiments were conducted on rat jejunum.
  • The study utilized cholera toxin and 5-HT to induce fluid secretion.
  • Inhibitory effects of 5-HT2 receptor antagonist (ketanserin) and 5-HT3 receptor antagonist (ICS 205-930) were assessed.

Main Results:

  • Both ketanserin and ICS 205-930 partially reduced cholera toxin-induced secretion in a dose-dependent manner.
  • Combined blockade of 5-HT2 and 5-HT3 receptors completely abolished cholera toxin-induced secretion.
  • This combined blockade did not affect cholera toxin-induced cyclic adenosine monophosphate increase or secretion induced by prostaglandin E2 and bisacodyl.

Conclusions:

  • 5-HT plays a significant role in cholera toxin-induced secretion.
  • A proposed model suggests cholera toxin induces 5-HT release, leading to prostaglandin E2 formation (via 5-HT2 receptors) and neuronal activation (via 5-HT3 receptors).
  • Combined 5-HT2 and 5-HT3 receptor blockade offers a potential strategy to inhibit cholera-induced fluid secretion.