ArticleFrontiers in pharmacology2016
Activation of Muscarinic Acetylcholine Receptor Subtype 4 Is Essential for Cholinergic Stimulation of Gastric Acid Secretion: Relation to D Cell/Somatostatin.
Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Somatostatin and Its Analogues as Second-Line Treatments in Non-Neoplastic Conditions.International journal of molecular sciences · 2026Review
- Agonists, Antagonists and Receptors of Somatostatin: Pathophysiological and Therapeutical Implications in Neoplasias.Current issues in molecular biology · 2024Review
- Managing gastrointestinal manifestations in systemic sclerosis, a mechanistic approach.Expert review of clinical immunology · 2024Review
- Neuroendocrine mechanism of gastric acid secretion: Historical perspectives and recent developments in physiology and pharmacology.Journal of neuroendocrinology · 2023Review
- Differential Actions of Muscarinic Receptor Subtypes in Gastric, Pancreatic, and Colon Cancer.International journal of molecular sciences · 2021Review
- CD36 maintains the gastric mucosa and associates with gastric disease.Communications biology · 2021Article
- Versatile Functions of Somatostatin and Somatostatin Receptors in the Gastrointestinal System.Frontiers in endocrinology · 2021Review
- The Physiology of the Gastric Parietal Cell.Physiological reviews · 2020Review
- Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease.Gastroenterology · 2019Review
- Centrally Administered Cortistation-14 Induces Antidepressant-Like Effects in Mice via Mediating Ghrelin and GABAFrontiers in pharmacology · 2018Article
- The Gastric and Intestinal Microbiome: Role of Proton Pump Inhibitors.Current gastroenterology reports · 2017Review
- Expression of M3 muscarinic acetylcholine receptors in gastric cancer.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieArticle
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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
BACKGROUND/
aimMuscarinic acetylcholine receptors exist in five subtypes (M1∼M5), and they are widely expressed in various tissues to mediate diverse autonomic functions, including gastric secretion. In the present study, we demonstrated, using M1∼M5 KO mice, the importance of M4 receptors in carbachol (CCh) stimulation of acid secretion and investigated how the secretion is modulated by the activation of M4 receptors.
methodsC57BL/6J mice of wild-type (WT) and M1-M5 KO were used. Under urethane anesthesia, acid secretion was measured in the stomach equipped with an acute fistula. CCh (30 μg/kg) was given subcutaneously (s.c.) to stimulate acid secretion. Atropine or octreotide (a somatostatin analog) was given s.c. 20 min before the administration of CCh. CYN154806 (a somatostatin SST2 receptor antagonist) was given i.p. 20 min before the administration of octreotide or CCh.
resultsCCh caused an increase of acid secretion in WT mice, and the effect was totally inhibited by prior administration of atropine. The effect of CCh was similarly observed in the animals lacking M1, M2 or M5 receptors but significantly decreased in M3 or M4 KO mice. CYN154806, the SST2 receptor antagonist, dose-dependently and significantly reversed the decreased acid response to CCh in M4 but not M3 KO mice. Octreotide, the somatostatin analog, inhibited the secretion of acid under CCh-stimulated conditions in WT mice. The immunohistochemical study showed the localization of M4 receptors on D cells in the stomach. Serum somatostatin levels in M4 KO mice were higher than WT mice under basal conditions, while those in WT mice were significantly decreased in response to CCh.
conclusionsThese results suggest that under cholinergic stimulation the acid secretion is directly mediated by M3 receptors and indirectly modified by M4 receptors. It is assumed that the activation of M4 receptors inhibits the release of somatostatin from D cells and minimizes the acid inhibitory effect of somatostatin through SST2 receptors, resulting in enhancement of the acid response mediated by M3 receptors on parietal cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.