[Ca²⁺]_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-InsP₃ in the apical region resulted in Ca²⁺ release from the apical trigger zone and after a latent period the initiation of an apical to basal Ca²⁺ wave. The latency was longer and the wave speed significantly slower in pancreatic compared to parotid cells. Focal photolysis in basal regions evoked only limited Ca²⁺ 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-Ca²⁺ failed to evoke a propagating Ca²⁺ wave in either cell type. However, the kinetics of the Ca²⁺ signal evoked following photolysis of caged-InsP₃ were significantly dampened by ryanodine in parotid but not pancreas, indicating a more prominent functional role for RyR following InsP₃R activation. These data suggest that differing expression levels of InsP₃R, RyR and possibly cellular buffering capacity may contribute to the fast kinetics of Ca²⁺ signals in parotid when compared to pancreas. These properties may represent a specialization of the cell type to effectively stimulate Ca²⁺-dependent effectors important for the differing primary physiological role of each gland.