Neural and hormonal control of membrane conductance in the pig pancreatic acinar cell.

Intracellular microelectrode recordings from superfused segments of pig pancreas have shown the resting acinar cell membrane potentials to range widely, with a mean value of -30.5 +/- 1.3 mV. Electrical field stimulation (FS) of the intrinsic pancreatic nerves induced frequency-dependent membrane hyperpolarization (10-15 mV) accompanied by a concomitant reduction in input resistance. Similar effects could be evoked by the superfusion or electroionophoresis of acetylcholine, amphibian or mammalian bombesin [gastrin-releasing peptide (GRP)], and pentagastrin. In normal Ca2+-containing solutions sustained secretagogue superfusion resulted in sustained hyperpolarization. In the absence of external Ca2+, similar stimulation caused only a transient hyperpolarizing response, with subsequent periods of secretagogue application having no effect. Atropine completely abolished the FS-evoked hyperpolarizations but had no effect on the responses evoked by bombesin, GRP, and pentagastrin. The present findings support the contention that neural and hormonal stimulation of the pig pancreas evokes Ca2+-dependent acinar cell hyperpolarization by causing a selective increase in membrane K+ permeability. A hypothesis is proposed that cellular K+ release through the opened conductance pathway promotes a K+-Na+-Cl- cotransport into the cell that serves a key function in the generation of acinar salt secretion.