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

1)细胞内Ca~(2+)拮抗剂TMB-8或细胞内Ca~(2+)螯合剂BAPTA-AM可显著抑制氨基甲胆碱(CCH)诱导的大鼠腮腺腺泡细胞K~+释放。联合加入离子霉素和thapsigargin后，[Ca~(2+)]迅速升高，K~(2+)明显释放。PMA不能增强CCH诱导的K~+释放。结果表明，[Ca~(2+)]_1的释放主要由[Ca~(^&lt；2+&gt；)_1的快速升高所介导，而与蛋白激酶的激活无关。PMA通过抑制肌醇磷脂的水解作用而减弱CCH诱导的[Ca~(2+)]_1的升高。蛋白激酶C的激活可能在大鼠腮腺腺泡细胞毒扁豆碱途径的负反馈控制中起作用。3)斯塔诺孢菌素增强大鼠腮腺腺泡细胞内钙储备耗竭所诱导的钙内流。相反，磷酸酶抑制剂抑制了钙离子的进入。上述结果提示，大鼠腮腺腺泡细胞的[Ca^&lt；2+&gt；2+]_1通道参与了磷酸化-去磷酸化机制的调节。4)外源性ATP可抑制M受体诱导的[Ca^&lt；2+&gt；]_1升高。

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.