Bradykinin-induced intracellular Ca2+ elevation in neuroblastoma X glioma hybrid NG108-15 cells; relationship to the action of inositol phospholipids metabolites.

The effect of bradykinin on the intracellular Ca2+ concentration ([Ca2+]i) in NG108-15 cells was studied using a Ca2+ indicator quin 2. Bradykinin induced two phases of change in [Ca2+]i. Bradykinin induced a spike phase of [Ca2+]i increase which was detectable within 15 s and decayed to near-basal concentration in 3 min and then a prolonged plateau phase of [Ca2+]i increase which continued for 15 min. The bradykinin-induced spike phase was not diminished by decreasing extracellular Ca2+ concentration ([Ca2+]o) to 1 microM. On the contrary, the plateau phase was dependent on [Ca2+]o and inhibited by Ca2+ blockers, verapamil (50 microM), nifedipine (1 microM). The iontophoretic injection of inositol-trisphosphate (IP3) into the single cell induced the increase of [Ca2+]i, which was independent of [Ca2+]o. These results indicate that the bradykinin-induced spike phase is mediated by the release of intracellular Ca2+ stores induced by IP3, while the plateau phase is mediated by influx of extracellular Ca2+ probably through voltage-sensitive Ca2+ channels.