The agonists acetylcholine (ACh) and cholecystokinin (CCK) evoke oscillating cytosolic Ca2+ signals in pancreatic acinar cells. Low agonist concentrations evoke local cytosolic Ca2+ spikes confined to the secretory pole region and intracellular inositol trisphosphate application can mimick this action. These spikes can occur alone, repetitively or precede longer lasting Ca2+ transients that spread throughout the cell. ACh and CCK evoke different Ca2+ signal patterns also influenced by the resting cytosolic Ca2+ concentration ([Ca2+]i). Ca2+ pump-mediated Ca2+ extrusion occurs in a pulsatile manner and is synchronous with the transient elevations of [Ca2+]i.