Molecular mechanism of the receptor-mediated Ca^<2+> entry in parotid cells

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1) Effects of the protein kinase inhibitor staurosporine on capacitative Ca^<2+> entry in rat parotid cells. Staurosporine significantly enhanced Ca^<2+> entry from extracellular medium activated by depletion of intracellular Ca^<2+> stores.2) Effects of serine/threonine phosphatase inhibitors on capacitative Ca^<2+> entry in rat parotid cells. The phosphatase inhibitors (calyculin-A, tautomycin, okadaic acid) suppressed the Ca^<2+> entry induced by depletion of intracellular Ca^<2+> stores.These results suggest that the capacitative Ca^<2+> entry may be regulated by protein phosphorylation/dephosphorylation.3) ATP-induced Ca^<2+> entry in rat parotid cells. Ectracellular ATP increased cytosolic Ca^<2+> concentration without formation of inositol phosphates. This increase appears to be due to an entry of Ca^<2+> via activation of P_<2Z> purinoceptors.4) Imaging of intracellular Ca^<2+> mobilizing in rat parotid acinar cells. When parotid acinus was stimulated with carbachol, the initial rise in cytosolic Ca^<2+> was detected in the apical pole of the cells. Thereafter, the increase spreaded into the basolateral area. When Ca^<2+> was added to the medium following depletion of intracellular Ca^<2+> stores, an increase in cytosolic Ca^<2+> was observed in the basal pole.5) Visualization of intracellular Ca^<2+> stores in a human parotid ductal cell line. The intracellular Ca^<2+> stores were visualized using digital imaging techniques with a confocal laser microscopy. The results demonstrate that the entire ER and the nuclear envelop serve as IP_3-sensitive Ca^<2+> stores.