title: Different implications of Ca2+i and and Ca2+e in CCK/gastrin-induced amylase secretion in AR4-2J cells.
abstract: The importance of Ca2+ in the regulation of secretion is well-known. However, recent experiments suggest that a rise in intracellular Ca2+ (Ca2+i) does not necessarily trigger secretion in pancreatic acinar cells. In AR4-2J cells the role of the Ca2+ mobilization induced by cholecystokinin/gastrin (CCK/G), which is dependent of the intracellular calcium store and the calcium influx operating through voltage-dependent calcium channels, has never been directly demonstrated. Therefore, we attempted to determine whether Ca2+i and/or extracellular Ca2+ (Ca2+e) mobilized by CCK/G plays a role in the amylase secretion of these cells. We measured the [Ca2+]i by spectrofluorometry and amylase release in different experimental procedures modulating the two pools of calcium. Ionomycin increased both [Ca2+]i and amylase related. In Ca(2+)-depleted cells or in the presence of thapsigargin the transient rise in Ca2+i and the amylase secretion induced by CCK/G were suppressed. A 50 mM K+ solution or Bay K 8644, which activated the Ca2+ influx, did not induce any variation of the basal amylase secretion. Moreover, amylase secretion induced by CCK/G did not change significantly in Ca(2+)-free medium or in the presence of nifedipine. These results indicate that in AR4-2J cells, amylase secretion is dependent of the large increase in Ca2+i induced by CCK/G and independent of the Ca2+ influx through voltage-dependent calcium channels dihydropyridine sensitive.
authors.affiliation: INSERM U151, Institut Fédératif de Recherches Louis Bugnard, CHU Rangueil, Toulouse, France.
authors.forename: V
authors.initials: V
authors.lastname: Bertrand
authors.forename: M J
authors.initials: MJ
authors.lastname: Bastie
authors.forename: N
authors.initials: N
authors.lastname: Vaysse
authors.forename: L
authors.initials: L
authors.lastname: Pradayrol
mesh_terms: D000681:Amylases / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D002766:Cholecystokinin / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005755:Gastrins / Q000494:pharmacology*; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism*; D015640:Ion Channel Gating; D015759:Ionomycin / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D010190:Pancreatic Neoplasms / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D013050:Spectrometry, Fluorescence; D013729:Terpenes / Q000494:pharmacology; D019284:Thapsigargin; D014407:Tumor Cells, Cultured
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D004791:Enzyme Inhibitors; D005755:Gastrins; D007476:Ionophores; D013729:Terpenes; D015759:Ionomycin; D019284:Thapsigargin; D002766:Cholecystokinin; D000681:Amylases; D009543:Nifedipine; D002118:Calcium