AJP - Gastrointestinal and Liver Physiology, Vol 245, Issue 4 499-G503, Copyright © 1983 by American Physiological Society
A transcellular route for Na-coupled Cl transport in secreting pancreatic acinar cells
J. O'Doherty and R. J. Stark
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.
