Regulation of parietal cell calcium signaling in gastric glands

The ligands interacting with enterochromaffin-like (ECL) and parietal cells and the signaling interactions between these cells were investigated in ra bbit gastric glands using confocal microscopy. Intracellular calcium concen tration ([Ca2+](i)) changes were used to monitor cellular responses. Histam ine and carbachol increased [Ca2+](i) in parietal cells. Gastrin (1 nM) inc reased [Ca2+](i) in ECL cells and adjacent parietal cells. Only the increas e of [Ca2+](i) in parietal cells was inhibited by H-2 receptor antagonists (H(2)RA). Gastrin (10 nM) evoked an H(2)RA-insensitive [Ca2+](i) increase i n parietal cells. Carbachol produced large H(2)RA- and somatostatin-insensi tive signals in parietal cells. Pituitary adenylate cyclase-activating pept ide (PACAP, 100 nM) elevated [Ca2+](i) in ECL cells and adjacent parietal c ells. H2RAs abolished the PACAP-stimulated [Ca2+](i) increase in adjacent p arietal cells. Somatostatin did not inhibit the increase of [Ca2+](i) in pa rietal cells stimulated with histamine, high gastrin concentrations, or car bachol but abolished ECL cell calcium responses to gastrin or PACAP. Hence, rabbit parietal cells express histaminergic, muscarinic, and CCK-B recepto rs coupled to calcium signaling but insensitive to somatostatin, whereas ra bbit and rat ECL cells express PACAP and CCK-B calcium coupled receptors se nsitive to somatostatin.