In the present study we have characterized receptor-mediated Ca2+ signalling patterns as well as Ca(2+)-mediated ion transport mechanisms in collagenase isolated rat pancreatic acini. Measurements of the initial Ca2+ response to maximal carbachol stimulation revealed a rapid increase in [Ca2+]i, which, in general, occurred synchronously throughout the cells. Less frequently, not all cells in the acinus responded to carbachol, but did respond to subsequent stimulation with bombesin, indicating that not all cells possess receptors for all the applied agonists. In view of the heterogeneity in the agonist-evoked Ca2+ responses, ionomycin was used to assess the role of Ca2+ in activating K+, Na+ and Cl- transport mechanisms, Ionomycin induced a rise in [Ca2+]i, thereby increasing Cl- permeability as well as stimulating K+ efflux, probably through non-specific cation channels. However, the resting K+ efflux was insensitive to blockers of non-specific cation channels, indicating the existence of a selective resting K+ conductance. Ionomycin also stimulated influx of Na+, which in part was mediated by non-specific cation channels. The changes in ion fluxes measured in the present study revealed that when [Ca2+]i is raised in rat pancreatic acini, they gain Na+ and Cl- and lose K+, with non-specific cation channels being essential for this process.