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 ([Ca2+]i) changes were used to monitor cellular responses. Histamine and carbachol increased [Ca2+]i in parietal cells. Gastrin (1 nM) increased [Ca2+]i in ECL cells and adjacent parietal cells. Only the increase of [Ca2+]i in parietal cells was inhibited by H2 receptor antagonists (H2RA). Gastrin (10 nM) evoked an H2RA-insensitive [Ca2+]i increase in parietal cells. Carbachol produced large H2RA- and somatostatin-insensitive signals in parietal cells. Pituitary adenylate cyclase-activating peptide (PACAP, 100 nM) elevated [Ca2+]i in ECL cells and adjacent parietal cells. H2RAs abolished the PACAP-stimulated [Ca2+]i increase in adjacent parietal cells. Somatostatin did not inhibit the increase of [Ca2+]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.