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1 Clinical Dental Sciences, The University of Liverpool, Liverpool, Merseyside, United Kingdom; The Physiology Laboratory, The University of Liverpool, Liverpool, Merseyside, United Kingdom
2 Clinical Dental Sciences, The University of Liverpool, Liverpool, Merseyside, United Kingdom
3 The Physiology Laboratory, The University of Liverpool, Liverpool, Merseyside, United Kingdom
* To whom correspondence should be addressed. E-mail: petesmif{at}liv.ac.uk.
Polarised Ca2+ signals, which originate at and spread from the apical pole, have been shown to occur in acinar cells from lacrimal, parotid, and pancreatic glands. However 'local' Ca2+ signals, that are restricted to the apical pole of the cell, have been previously demonstrated only in pancreatic acinar cells where the primary function of the Ca2+ signal is to regulate exocytosis. We show that submandibular acinar cells, where the primary function of the Ca2+ signal is to drive fluid and electrolyte secretion, are capable of both Ca2+ waves and local Ca2+ signals. The generally accepted model for fluid and electrolyte secretion requires simultaneous Ca2+-activation of basally located K+ channels and apically located Cl- channels. Whereas a propagated cell-wide Ca2+ signal is clearly consistent with this model, a 'local' Ca2+ signal is not, because there is no increase in [Ca2+]i at the basal pole of the cell. Our data provide the first direct demonstration, in submandibular acinar cells, of the apical and basal location of the Cl- and K+ channels respec tively and confirm that 'local' Ca2+ signals do not Ca2+-activate K+ channels. We re-evaluate the model for fluid and electrolyte secretion and demonstrate that Ca2+-activation of the Cl- channels is sufficient to voltage-activate the K+ channels and thus demonstrate that 'local' Ca2+ signals are sufficient to support fluid secretion.
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