ArticleAnnals of the New York Academy of Sciences2000
Role of PACAP1 receptor in regulation of ECL cells and gastric acid secretion by pituitary adenylate cyclase activating peptide.
Article in Annals of the New York Academy of Sciences, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 24 citations in OpenAlex.
- Sensory neuron regulation of gastrointestinal inflammation and bacterial host defence.Journal of internal medicine · 2017Review
- Vasoactive intestinal peptide/pituitary adenylate cyclase activating polypeptide, and their receptors and cancer.Current opinion in endocrinology, diabetes, and obesity · 2016Review
- Physiological and clinical significance of enterochromaffin-like cell activation in the regulation of gastric acid secretion.World journal of gastroenterology · 2007Review
- PAC1 and PACAP expression, signaling, and effect on the growth of HCT8, human colonic tumor cells.Regulatory peptides · 2002Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
We previously reported that PAC1 is expressed on ECL cells resulting in stimulation of [Ca2+]i, histamine and acid secretion. The study reported here characterized the signaling by PAC1 on ECL cells; determined the effects of PACAP on the gastric acid secretion in vivo, and determined the effects of chronic administration of PACAP-27 on ECL cell proliferation. PACAP-27 dose dependently stimulated ECL cell Ca2+ and AC with detectable stimulation at 1 nM and maximal stimulation at 100 nM (six-fold). In rats PACAP-27 administration (10 pmol/kg/h) increased the rate of gastric acid secretion when an antisomatostatin antibody was co-administered. Chronic administration of PACAP (10 pmol/h for seven days) via osmotic pump resulted in a more than twofold increase in BrdU incorporation into ECL cells. PACAP acting at the PAC1 results in dual signaling responses to both [Ca2+]i. AC in ECL cells stimulates gastric acid secretion via the actions of histamine acting at the parietal cell and in whole animals leads to proliferation of ECL cells when administered chronically.
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