The cross-talk and secretion in intracellular signaling in parotid glands

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1) Treatment with the intracellular Ca^<2+> antagonist TMB-8 or the intracellular Ca^<2+> chelator BAPTA-AM strongly suppressed the carbachol (CCh)-induced K^+ release from rat parotid acini. Combined addition of ionomycin anf thapsigargin caused a rapid increas in [Ca^<2+>] and resulted in a marked release of K^+. PMA did not potenciate the CCh-induced K^+ release. The results indicate that the K^+ release is prrimarily mediated by a rapid increase in [Ca^<2+>]_1 but is not associated with activation of proteon kinase C.2) PMA attenuated the CCh-induced increase in [Ca^<2+>]_1 through inhibition of phosphoinositide hydrolysis. Activation of protein kinase C may play a role in negative-feedback control of the muscarinic pathway in rat parotid acinar cells.3) Staurosporine enhanced Ca^<2+> entry induced by depletion of intracellular Ca^<2+> stores in rat parotid acinar cells. By contrast, the phosphatase inhibitors suppressed the Ca^<2+> entry. The results suggest that phosphorylation-dephosphorylation mechanism is involeved in the regulation of the capacitative Ca^<2+> entry.4) The increase in [Ca^<2+>]_1 induced through muscarinic receptors was inhibited by external ATP.This result suggests that is a cross-talk mechanism between muscarinic receptors and purinergic ones in rat parotid acinar cells.