Effects of bradykinin on Ca 2+ mobilization and prostaglandin E 2 release in human periodontal ligament cells.

In fura‐2‐loaded human periodontal ligament (HPDL) cells, bradykinin induced a rapidly transient increase and subsequently sustained increase in cytosolic Ca 2+ ([Ca 2+ ] i ). When external Ca 2+ was chelated by EGTA, the transient peak of [Ca 2+ ] i was reduced and the sustained level was abolished, implying the Ca 2+ mobilization consists of intracellular Ca 2+ release and Ca 2+ influx. Thapsigargin, a specific Ca 2+ ‐ATPase inhibitor for inositol 1,4,5‐trisphosphate (1,4,5‐1P 3 )‐sensitive Ca 2+ pool, induced an increase in [Ca 2+ ] i in the absence of external Ca 2+ . After depletion of the intracellular Ca 2+ pool by thapsigargin, the increase in [Ca 2+ ] i induced by bradykinin was obviously reduced. Bradykinin also stimulated formation of inositol polyphosphates including 1,4,5‐IP 3 . These results suggest that bradykinin stimulates intracellular Ca 2+ release from the 1,4,5‐1P 3 ‐sensitive Ca 2+ pool. Bradykinin stimulated prostaglandin E 2 (PGE 2 ) release in the presence of external Ca 2+ , but not in the absence of external Ca 2+ . Ca 2+ ionophore A23187 and thapsigargin evoked the release of PGE 2 in the presence of external Ca 2+ despite no activation of bradykinin receptors. These results indicate that bradykinin induces Ca 2+ mobilization via activation of phospholipase C and PGE 2 release caused by the Ca 2+ influx in HPDL cells.