ArticleBritish journal of pharmacology2004
Calcitonin gene-related peptide facilitates serotonin release from guinea-pig colonic mucosa via myenteric neurons and tachykinin NK2/NK3 receptors.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Neuropeptide-induced modulation of carcinogenesis in a metastatic breast cancer cell line (MDA-MB-231Cancer cell international · 2018Article
- An Endogenous Tachykinergic NK2/NK3 Receptor Cascade System Controlling the Release of Serotonin from Colonic Mucosa.Current neuropharmacology · 2015Review
- A role for endogenous peptide YY in tachykinin NK(2) receptor-triggered 5-HT release from guinea pig isolated colonic mucosa.British journal of pharmacology · 2012Article
- Melatonin inhibits tachykinin NK₂ receptor-triggered 5-HT release from guinea pig isolated colonic mucosa.British journal of pharmacology · 2011Article
- Autonomic nervous system and secretion across the intestinal mucosal surface.Autonomic neuroscience : basic & clinical · 2007Review
- Calcitonin-secreting VIPoma.Digestive diseases and sciences · 2005Article
- Tachykinin NK2 receptor antagonists for the treatment of irritable bowel syndrome.British journal of pharmacology · 2004Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of calcitonin gene-related peptide (CGRP), to alter the outflow of 5-hydroxytryptamine (5-HT) from the guinea-pig proximal colon, was evaluated using three different isolated preparations: whole colon, mucosa-free muscle layer and submucosa/mucosa preparations. In the presence of the monoamine oxidase A inhibitor, clorgyline, CGRP elicited a concentration-dependent increase in 5-HT outflow from the whole colon, but not from mucosa-free muscle layer preparations. The CGRP-evoked 5-HT outflow was sensitive to tetrodotoxin (TTX) or hexamethonium, but was not detectable in submucosa/mucosa preparations. HCGRP8-37 (3 microM) inhibited the submaximal effect of CGRP on the 5-HT outflow. [Cys(ACM)2,7]hCGRP had a slight stimulant influence on the 5-HT outflow. The selective NK2 and NK3 receptor antagonists, SR48968 or SR142801, respectively, prevented the enhancing effect of CGRP. By contrast, a selective NK1 receptor antagonist L703606, failed to block the effect of CGRP. The enhancing effect of CGRP was mimicked by the NK2 receptor agonist [beta-Ala8]-neurokinin A (NKA)4-10 and the NK3 receptor agonist senktide. The effect of [beta-Ala8]-NKA4-10 on the 5-HT outflow was unaffected by TTX, while the effect of senktide was prevented by TTX, hexamethonium or SR48968. The present data also demonstrated a synergistic action of the NK2 and NK3 receptor agonists on the CGRP-evoked 5-HT outflow. We concluded that CGRP facilitates 5-HT release from the guinea-pig colonic mucosa through an action on myenteric neurons and that this effect is mediated by endogenously released tachykinins, acting via tachykinin NK2/NK3 receptors in cascade. British Journal of Pharmacology (2004) 141, 385-390. doi:10.1038/sj.bjp.0705624
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