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Carbachol‐induced [Ca2+]i increase, but not activation of protein kinase C, stimulates exocytosis in rat parotid acini

A column perfusion system was applied to rat parotid acinar cells to clarify the roles of Ca2+ and protein kinase C (PKC) in the mechanisms of carbachol (CCh)‐induced amylase secretion. CCh evoked a biphasic response of amylase secretion with an initial rapid and large peak that reached maximum at about 10 s followed by a sustained plateau. The time profile and the dose‐response relationship paralleled with those of cytosolic free Ca2+ concentration ([Ca2+]i). The CCh‐induced sustained response of amylase secretion maintained by Ca2+ influx into cells was ATP dependent, while the initial peak response regulated by Ca2+ released from InsP3‐sensitive stores was relatively ATP independent. Restoration of extracellular Ca2+ during continuous stimulation with CCh in Ca2+‐free medium evoked a second rapid and large peak of amylase secretion. Phorbol 12,13‐dibutyrate (PDBu) potentiated the CCh‐induced amylase secretion in both the initial peak and the sustained plateau without enhancing CCh‐induced [Ca2+]i changes. PKC inhibitors such as Ro 31–8220 inhibited the potentiating effect of PDBu but only slightly reduced amylase secretion induced by CCh alone. These results suggest that a CCh‐induced rise in [Ca2+]i triggers the final fusion and/or exocytosis of amylase secretion. CCh also has some ability to promote ATP‐dependent priming of secretory granules that, together with Ca2+ influxed into cells, contributes to the CCh‐induced sustained plateau of amylase secretion. PDBu‐induced activation of PKC promotes the priming of secretory granules, thereby enhancing the efficacy for Ca2+ to trigger fusion/exocytosis.