Previous studies have claimed that acetylcholine-induced NaCl secretion in pancreatic acinar cells occurs via the so-called ‘push-pull’ concept, whereby in the first (‘push’) phase Cl– is extruded across the luminal membrane, and Na+ and Cl– are taken up across the basolateral membrane in the second (‘pull’) phase via nonselective and Cl- channels. We have examined this issue recently with micromolar carbachol (CCH) concentrations in rat pancreatic acinar cells and concluded that the ‘push-pull’ model can probably not account for NaCl and fluid excretion under these conditions. In micromolar concentrations CCH induces strong and usually stable depolarization to values close to the predicted Nernst potential of Cl–. In the present study we have repeated and expanded previous experiments but have used very low (50 nmol/l) concentrations of CCH. At these concentrations Vm depolarized in oscillating fashion (ca. 0.2 Hz) from -48 ± 1.7 to -36 ± 1.7 mV (n = 33). In the absence of Na+ (NMDG+ replacement), CCH induced oscillating depolarizations from -59 ± 3.3 to -44 ± 2.5 mV (n = 37). The Vm oscillations followed Ecι-. Whole cell conductance was maximal during CCH-induced depolarizations (close to Ecl-) and minimal with stable and hypolarized Vm, approaching the Nernst potential for a nonselective cation channel (n = 26). These data suggest that the ‘push-pull’ model is unlikely to account for CCH-induced NaCl secretion in these cells.

Journal Section:
Original Paper
Keywords:
NaCl secretion, Pancreas, Carbachol, Cl– conductance, Voltage oscillations
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© 1996 S. Karger AG, Basel
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1996
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