The role of calcium in agonist-stimulated hydrolysis of phosphatidylinositol in mouse pancreas.
The effects of Ca2+ on agonist-stimulated hydrolysis of myo-[2-3H]inositol-labelled phosphatidylinositol in mouse pancreas in vitro, were studied. The increase in cytosol Ca2+ concentration produced by the ionophore A23187 did not stimulate the breakdown of phosphatidylinositol. Cholecystokinin-octapeptide (CCK-8) stimulated the hydrolysis of phosphatidylinositol under conditions in which intracellular calcium stores were depleted. The breakdown of phosphatidylinositol was stimulated by bethanechol and CCK-8 in Ca2+ -free Krebs solution, and the addition of Ca2+ to the medium potentiated the effects of these agonists. Lanthanum significantly reduced bethanechol and CCK-8-stimulated hydrolysis of phosphatidylinositol in Krebs solution, but was without effect in Ca2+ -free Krebs solution. The results of this study support the proposal that hydrolysis does not occur as a result of Ca2+ mobilization and may be involved in Ca2+ gating in the pancreas.
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001067:Appetite Depressants / Q000494:pharmacology; D018723:Bethanechol; D001626:Bethanechol Compounds / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002766:Cholecystokinin / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D007700:Kinetics; D007811:Lanthanum / Q000494:pharmacology; D051379:Mice; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism*; D010446:Peptide Fragments / Q000494:pharmacology; D010716:Phosphatidylinositols / Q000378:metabolism*; D012844:Sincalide
D000900:Anti-Bacterial Agents; D001067:Appetite Depressants; D001626:Bethanechol Compounds; D010446:Peptide Fragments; D010716:Phosphatidylinositols; D018723:Bethanechol; D000001:Calcimycin; D007811:Lanthanum; D002766:Cholecystokinin; D012844:Sincalide; D002118:Calcium