Involvement of serotonin and calcium channels in the intestinal fluid secretion evoked by bile salt and cholera toxin
Open accessAbstract
The enteric nervous system (ENS) is activated when exposing the intestinal mucosa to cholera toxin or certain bile salts. Cholera toxin stimulates ENS, at least in part, by the release of 5‐hydroxytryptamine (5‐HT) from the enterochromaffin cells. Calcium channel blockers of the L‐type markedly attenuate the fluid secretion and the luminal release of 5‐HT caused by cholera toxin. The objective of the present study was to elucidate if sodium deoxycholate activated ENS in a similar manner as cholera toxin. Furthermore, the effect of several calcium channel blockers was tested on the fluid secretion caused by cholera toxin or bile salt. Sodium deoxycholate (4 m M ) caused a release of 5‐HT into the intestinal lumen, which was inhibited by calcium channel blockade. Granisetron, a 5‐HT 3 receptor blocker, partly inhibited the fluid secretion caused by bile salt. The effects of nifedipine, felodipine, R‐felodipine, H186/86 ( t ‐butyl analogue of felodipine) on the fluid secretion caused by cholera toxin or sodium deoxycholate were studied. Both secretory states were markedly attenuated in a dose dependent manner by all calcium channel blockers tested regardless of their effects on arterial pressure. It is concluded that both cholera toxin and bile salt activate ENS, at least in part, via a release of 5‐HT from the enterochromaffin cells. The antisecretory effect calcium channel blockers is partly explained by an inhibition of this release of 5‐HT. British Journal of Pharmacology (1999) 127 , 887–894; doi: 10.1038/sj.bjp.0702615
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Enterochromaffin cells secrete serotonin and signaling peptides in response to various physiological and pathological luminal stimuli, such as microbial factors or bacterial toxins, as well as central stimuli.
“Enterochromaffin cells secrete serotonin and signaling peptides (for example, corticotropin-releasing hormone, cholecystokinin and somatostatin) in response to various physiological and pathological luminal stimuli,53-55 such as microbial factors or bacterial toxins,56-58 as well as central stimuli (see discussion above).31,32”
From Principles and clinical implications of the brain-gut-enteric microbiota axis (2009) · cites this paper as [57]
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- Authors
- Peregrin, A. T., Ahlman, H., Jodal, M., & Lundgren, O.
- Affiliations
- University of Gothenburg (SE)
- Corresponding author
- Lundgren, Ove
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 1999-06
- Volume
- 127
- Issue
- 4
- Pages
- 887-894
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC1566091
- OpenAlex
- W2057090803
- Cited by
- 71
- References
- 41
- Citations by year
- 2025: 2 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 4 · 2016: 3 · 2015: 1 · 2014: 4 · 2013: 3 · 2012: 5
- FWCI
- 2.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Keywords
- serotonin, calcium channels, L-type calcium channel blockers, enteric nervous system, intestinal secretion, bile salts, sodium deoxycholate, cholera toxin, enterochromaffin cells, serotonin release, granisetron, nifedipine, felodipine, antisecretory effect
- MeSH terms
- Animals, Bile Acids and Salts, Cholera Toxin, Intestinal Mucosa, Male, Nifedipine, Serotonin, Calcium Channels, Felodipine, Rats, Sprague-Dawley, Granisetron, Rats
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