Intracellular calcium concentration ([Ca(2+)](i)) signals are central to the mechanisms underlying fluid and protein secretion in pancreatic and parotid acinar cells. Calcium release was studied in natively buffered cells following focal laser photolysis of caged molecules. Focal photolysis of caged-inositol 1,4,5 trisphosphate (InsP(3)) in the apical region resulted in Ca(2+) release from the apical trigger zone and, after a latent period, the initiation of an apical-to-basal Ca(2+) wave. The latency was longer and the wave speed significantly slower in pancreatic compared with parotid cells. Focal photolysis in basal regions evoked only limited Ca(2+) release at the photolysis site and never resulted in a propagating wave. Instead, an apical-to-basal wave was initiated following a latent period. Again, the latent period was significantly longer under all conditions in pancreas than parotid. Although slower in pancreas than parotid, once initiated, the apical-to-basal wave speed was constant in a particular cell type. Photo release of caged-Ca(2+) failed to evoke a propagating Ca(2+) wave in either cell type. However, the kinetics of the Ca(2+) signal evoked following photolysis of caged-InsP(3) were significantly dampened by ryanodine in parotid but not pancreas, indicating a more prominent functional role for ryanodine receptor (RyR) following InsP(3) receptor (InsP(3)R) activation. These data suggest that differing expression levels of InsP(3)R, RyR, and possibly cellular buffering capacity may contribute to the fast kinetics of Ca(2+) signals in parotid compared with pancreas. These properties may represent a specialization of the cell type to effectively stimulate Ca(2+)-dependent effectors important for the differing primary physiological role of each gland.