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HORMONES AND SIGNALING

Local and global calcium signals and fluid and electrolyte secretion in mouse submandibular acinar cells

¹Clinical Dental Sciences, The University of Liverpool, The Edwards Building, Liverpool; and ²The Physiological Laboratory, The University of Liverpool, Liverpool, United Kingdom

Submitted 5 March 2004 ; accepted in final form 4 August 2004

Polarized Ca²⁺ signals that 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 in which the primary function of the Ca²⁺ signal is to regulate exocytosis. We show that submandibular acinar cells, in which 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 intracellular Ca²⁺ concentration 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, respectively, and confirm that local Ca²⁺ signals do not Ca²⁺-activate K⁺ channels. We reevaluate 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.

Ca²⁺ mobilization; patch-clamp; K⁺ channel; Cl^– channel

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