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1 Division of Gastroenterology, Department of Medicine, University of California, San Diego, San Diego, CA, USA
* To whom correspondence should be addressed. E-mail: kbarrett{at}ucsd.edu.
In previous studies we have found that 5-hydroxytryptamine (5-HT) is a potent
stimulant of duodenal mucosal bicarbonate secretion (DMBS) in mice. The aim of the
present study was to determine the intracellular signaling pathways and 5-HT receptor
subtypes involved in 5-HT-induced DMBS. Bicarbonate secretion by murine duodenal
mucosa was examined in vitro in Ussing chambers. 5-HT receptor involvement in DMBS
was inferred from pharmacologic studies using selective 5-HT receptor antagonists and
agonists. The expression of 5-HT4 receptor mRNA in duodenal mucosa and epithelial
cells was analyzed by RT-PCR. cAMP-dependent signaling pathway inhibitors MDL
12330A, Rp-cAMP, and H-89, and Ca2+-dependent signaling pathway inhibitors
verapamil and W-13 markedly reduced 5-HT-stimulated duodenal bicarbonate secretion
and Isc, whereas cGMP-dependent signaling pathway inhibitors NS2028 and KT5823
failed to alter these responses. Both SB204070 and ICS205.930 (selective 5-HT4
receptor antagonists) markedly inhibited 5-HT-stimulated bicarbonate secretion and Isc,
whereas methiothepine (5-HT1 receptor antagonist), ketanserin (5-HT2 receptor
antagonist), and a low concentration of ICS205.930 (5-HT3 receptor antagonist) had no
effect. RS67506 (partial 5-HT4 receptor agonist) concentration-dependently increased
bicarbonate secretion and Isc, whereas 5-carboxamidotryptamine (5-HT1 receptor
agonist), 
-methyl-5-HT (5-HT2 receptor agonist), and phenylbiguanide (5-HT3 receptor
agonist) did not significantly increase bicarbonate secretion or Isc. RT-PCR analysis
confirmed the expression of 5-HT4 receptor mRNA in murine duodenal mucosa and
epithelial cells. These results demonstrate that 5-HT regulates DMBS via both cAMP- and Ca2+-dependent signaling pathways and 5-HT4 receptors located in the duodenal
mucosa and/or epithelial cells.
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