Pancreatic acinar cells: acetylcholine‐induced membrane depolarization, calcium efflux and amylase release

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Abstract
1. The effects of acetylcholine upon the output of amylase, Ca2+ efflux and membrane potential of pancreatic acinar cells have been measured in segments of mouse pancreas superfused in vitro.2. Amylase output was measured continuously using an on‐line automated fluorimetric method; Ca2+ efflux was monitored by measuring the release of 45Ca2+ from pre‐labelled tissue; and intracellular recordings of acinar transmembrane potentials were obtained with glass micro‐electrodes. In some experiments membrane potentials, and in others 45Ca2+ efflux, were measured concomitantly with amylase release.3. Acetylcholine depolarized the acinar cells, increased tissue 45Ca2+ efflux and raised amylase output, each with a similar dose‐dependence, i.e. a maximal response at 10−5 M, threshold ⋜ 10−8 M, and ED50 values of 0·7 × 10−7 M, 0·5 × 10−7 M, and 2 × 10−7 M for depolarization, amylase release, and 45Ca2+ efflux, respectively.4. In response to acetylcholine both depolarization and 45Ca2+ efflux preceded or coincided with the increase in amylase output.5. Acetylcholine 10−5 M and [K]0 47 m M were without effect on 45Ca2+ efflux in the presence of atropine (3 × 10−6 M) but pancreozymin (0·3 u./ml.) still elicited a marked increase in 45Ca2+ release.6. These results suggest that the stimulatory action of acetylcholine on the pancreatic acinar cell involves, sequentially, a specific receptor‐activated increase in membrane permeability, depolarization, Ca2+ mobilization and amylase release. These events are discussed in relation to the integrated mechanism of stimulus‐secretion coupling.