Pancreatic acinar cells: electrophysiological evidence for stimulant‐evoked increase in membrane calcium permeability in the mouse.

Abstract

Membrane potential and resistance were measured in acini from superfused isolated segments of mouse pancreas using 2 micro-electrodes inserted into neighboring acinar cells. Stimulation was carried out exposing segments to 5 .times. 10-7 M-acetylcholine (ACh) or 3 .times. 10-7 M-pentagastrin. Sustained stimulation with ACh or pentagastrin caused sustained membrane depolarization and resistance reduction. For periods of stimulation up to 15 min there was no sign of desensitization. Sustained stimulation during exposure of the tissue to a Ca-free solution containing EGTA (ethyleneglycol bis-(.beta.-aminoethyl ether)-N,N''-tetraacetic acid) resulted only in a transient depolarization and resistance reduction. Removal of external Ca during sustained stimulation resulted in immediate hyperpolarization and increase in resistance. Readmission of Ca, still during exposure to ACh or pentagastrin, depolarized the membrane and reduced the resistance. Mn could not mimic this effect of Ca. Removal of external Ca in the absence of stimulation evoked depolarization and membrane resistance reduction. Sustained stimulation of pancreatic acinar cells with cholinergic agents or peptides of the cholecystokinin-gastrin group may evoke an increase in the Ca permeability of the plasma membrane. Ca entering the cells from the outside is important in maintaining ion channels in their open state, thus sustaining the stimulant-evoked depolarization and resistance reduction. The initial stimulant-evoked membrane response seems to be triggered by release of Ca from internal stores and is independent of external Ca.