Pancreatic acinar cells: ionic dependence of the membrane potential and acetylcholine‐induced depolarization

Abstract

1. Intracellular recordings of membrane potentials have been made in vitro from the exocrine acinar cells of the mouse pancreas using glass micro-electrodes.2. The mean membrane potential of the acinar cells during superfusion with Krebs-Henseleit solution was -39.2 mV. Increasing [K](o) tenfold decreased the membrane potential by 28 mV when [K](o) was above 10 mM. This depolarization was not affected by atropine (1.4 x 10(-6)M). Strophanthin-G (10(-3)M) slowly depolarized the cells at about 10 mV hr(-1).3. Brief exposure to acetylcholine (ACh), 5.5 x 10(-5)M, or pancreozymin resulted in a short lasting depolarization of the acinar cells. Atropine (1.4 x 10(-6)M) blocked the depolarizing action of ACh but not that of pancreozymin. Adrenaline (5.5 x 10(-5)M) or cyclic AMP (10(-3)-10(-4)M) did not influence the membrane potential.4. The amplitude of the ACh-induced depolarization was not dependent on the presence of CO(2)/HCO(3) in the bathing fluid, but it was closely dependent on the extracellular Na concentration. However, ACh was still able to evoke a small depolarization even after prolonged exposure of the tissue to a Na-free solution.5. During exposure of the tissue to a Ca-free solution the resting membrane potential was decreased and the ACh-induced depolarization was significantly reduced. Some substances which are known in other tissues to inhibit membrane Ca(2+) currents, i.e. La(3+), D-600 and tetracaine, were able to reduce, but never abolish, the ACh-induced depolarization.6. These results suggest that the effect of ACh on the pancreatic acinar cell is to increase the permeability of the membrane to commonly occurring ions with a consequent Na-influx and a small Ca-influx.