EFFECTS OF BRADYKININ ON CA2-LIGAMENT CELLS( MOBILIZATION AND PROSTAGLANDIN E(2) RELEASE IN HUMAN PERIODONTAL)

In fura-2-loaded human periodontal ligament (HPDL) cells, bradykinin i nduced a rapidly transient increase and subsequently sustained increas e in cytosolic Ca2+ ([Ca2+](i)). When external Ca2+ was chelated by EG TA, the transient peak of [Ca2+](i) was reduced and the sustained leve l was abolished, implying the Ca2+ mobilization consists of intracellu lar Ca2+ release and Ca2+ influx. Thapsigargin, a specific Ca2+-ATPase inhibitor for inositol 1,4,5-trisphosphate (1,4,5-IP3)-sensitive Ca2 pool, induced an increase in [Ca2+](i) in the absence of external Ca2 +. After depletion of the intracellular Ca2+ pool by thapsigargin, the increase in [Ca2+](i) induced by bradykinin was obviously reduced. Br adykinin also stimulated formation of inositol polyphosphates includin g 1,4,5-IP3. These results suggest that bradykinin stimulates intracel lular Ca2+ release from the 1,4,5-IP3-sensitive Ca2+ pool. Bradykinin stimulated prostaglandin E(2) (PGE(2)) release in the presence of exte rnal Ca2+, but not in the absence of external Ca2+. Ca2+ ionophore A23 187 and thapsigargin evoked the release of PGE(2) in the presence of e xternal Ca2+ despite no activation of bradykinin receptors. These resu lts indicate that bradykinin induces Ca2+ mobilization via activation of phospholipase C and PGE(2) release caused by the Ca2+ influx in HPD L cells.