A transcellular route for Na-coupled Cl transport in secreting pancreatic acinar cells.

Abstract

Ion-selective microelectrodes were employed to determine the electrochemical driving forces involved in the transepithelial transport of Na+ and Cl- during acetylcholine (ACh) stimulation of pancreatic acinar cells. In HCO-3-free Ringer solution, the mean values of intracellular Cl and Na activities (aiCl and aiNa) were 68.9 +/- 1.1 and 8.3 +/- 0.3 mM, respectively. The mean value of aiCl is above the calculated equilibrium value, indicating that Cl entry into the cell is an energy-requiring process. Continuous measurement of intracellular electrode potentials during stimulation of the cells with concentrations of ACh ranging from 10(-7) to 10(-5) M demonstrated the neurotransmitter's influence on transmembrane Na+ and Cl- movement in secreting cells. The mean values of the induced changes in aiCl and aiNa at every concentration of ACh measured were not significantly different (P greater than 0.5), although the mean changes in either aiNa or aiCl determined with every decade change in ACh concentration were significant (P less than 0.05). The transmembrane Na+ electrochemical gradient dissipated with the induced increases in aiCl. These results suggest that, during stimulus-secretion coupling of pancreatic acinar cells, there is a transcellular route for NaCl secretion, and the energy for NaCl entry into the cell may be derived from the Na+ electrochemical gradient that exists across the basolateral epithelial membrane. They also suggest that the ACh-induced changes in ionic permeability of the plasma membrane may be the coupling mechanism by which the simultaneous events enzyme release and electrolyte secretion are controlled in stimulated cells.