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

Content Provider	PubMed Central
Author	Yoshimura, Keiichi Murakami, Masataka Segawa, Akihisa
Copyright Year	2000
Abstract	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 InsP 3-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.
Related Links	http://dx.doi.org/10.1111/j.1469-7793.2000.t01-1-00403.x
Ending Page	416
Page Count	14
Starting Page	403
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 3
Volume Number	522
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2000-02-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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