Receptor‐mediated activation of neutrophils (PMN) initiates possibly interdependent events, including a rapid transient increase in [Ca²⁺]_i, implicated as a second messenger. To investigate whether this transient is required for eventual degranulation, PMN were incubated with an intracellular Ca²⁺ chelator (BAPTA), then exposed to chemotactic peptide [N‐formyl‐methionyl‐leucyl‐phenylalanine (fMLP)] with or without cytochalasin B (CB) or to high‐valency immune complexes (HIC); δ[Ca²⁺]_i, δpH_i, oxidative burst, and elastase release were then evaluated (plus or minus EGTA 15 s before stimulation) after 2 and 15 min incubation in 0.9 mM Ca²⁺. With either fMLP plus CB or HIC stimulation, BAPTA‐treated cells were unable to achieve a Ca²⁺ transient with a 2‐min incubation, whereas a 15‐min incubation allowed the BAPTA‐treated cells to recover a portion of the δ[Ca²+]_i. Even though BAPTA‐treated cells were unable to mount a δ[Ca²⁺]_i at 2 min, HIC‐stimulated BAPTA‐treated cells were able to elicit an oxidative burst (33% of control) and degranulation (67% of control). Therefore, we conclude that δ[Ca²⁺]_i modulates but is not required for oxidative burst or degranulation. J. Leukoc. Biol. 62: 329–340; 1997.