title: Regulation of parietal cell calcium signaling in gastric glands.
abstract: The ligands interacting with enterochromaffin-like (ECL) and parietal cells and the signaling interactions between these cells were investigated in rabbit gastric glands using confocal microscopy. Intracellular calcium concentration ([Ca(2+)](i)) changes were used to monitor cellular responses. Histamine and carbachol increased [Ca(2+)](i) in parietal cells. Gastrin (1 nM) increased [Ca(2+)](i) in ECL cells and adjacent parietal cells. Only the increase of [Ca(2+)](i) in parietal cells was inhibited by H(2) receptor antagonists (H(2)RA). Gastrin (10 nM) evoked an H(2)RA-insensitive [Ca(2+)](i) increase in parietal cells. Carbachol produced large H(2)RA- and somatostatin-insensitive signals in parietal cells. Pituitary adenylate cyclase-activating peptide (PACAP, 100 nM) elevated [Ca(2+)](i) in ECL cells and adjacent parietal cells. H(2)RAs abolished the PACAP-stimulated [Ca(2+)](i) increase in adjacent parietal cells. Somatostatin did not inhibit the increase of [Ca(2+)](i) in parietal cells stimulated with histamine, high gastrin concentrations, or carbachol but abolished ECL cell calcium responses to gastrin or PACAP. Hence, rabbit parietal cells express histaminergic, muscarinic, and CCK-B receptors coupled to calcium signaling but insensitive to somatostatin, whereas rabbit and rat ECL cells express PACAP and CCK-B calcium coupled receptors sensitive to somatostatin.
authors.affiliation: Department of Physiology, University of California, Los Angeles, West Los Angeles Healthcare Center, Los Angeles, California 90073, USA.
authors.forename: C
authors.initials: C
authors.lastname: Athmann
authors.forename: N
authors.initials: N
authors.lastname: Zeng
authors.forename: D R
authors.initials: DR
authors.lastname: Scott
authors.forename: G
authors.initials: G
authors.lastname: Sachs
mesh_terms: D000818:Animals; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D019861:Enterochromaffin-like Cells / Q000378:metabolism; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D005755:Gastrins / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D006728:Hormones / Q000494:pharmacology; D018613:Microscopy, Confocal; D008934:Mitogens / Q000494:pharmacology; D009479:Neuropeptides / Q000494:pharmacology; D010295:Parietal Cells, Gastric / Q000378:metabolism*; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide; D011817:Rabbits; D011899:Ranitidine / Q000494:pharmacology; D013004:Somatostatin / Q000494:pharmacology; D013047:Specific Pathogen-Free Organisms
chemical_list: D018679:Cholinergic Agonists; D005755:Gastrins; D006635:Histamine H2 Antagonists; D006728:Hormones; D008934:Mitogens; D009479:Neuropeptides; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide; D013004:Somatostatin; D006632:Histamine; D011899:Ranitidine; D002217:Carbachol