ABSTRACT
Aim: The purpose of this study was to observe the effect of 15-HETE on rabbit pulmonary artery (PA) vasoconstriction after removing extracellular Ca2+ and on [Ca2+]i in PASMCs and to discuss the mechanisms of cytosolic Ca2+ mobilization induced by 15-HETE. Methods: We used tention studies of PA rings to observe the effect of L-type Ca2+ channel blocker and non-Ca2+ solution on PA vasoconstriction induced by 15-HETE. Then we used laser-scanning confocal microscope to investigate [Ca2+]i signaling in cultured PASMCs. Results: L-type Ca2+ channel blocker and non-Ca2+ solution had no effect on 15-HETE induced vasoconstriction in normoxic and hypoxic rabbit PA rings. The increase of [Ca2+]i was shown in 15-HETE group cells and the change in [Ca2+]i induced by 15-HETE was significantly different from that of control. Conclusion: 15-HETE may activate Ca2+ release from intracellular stores and raise [Ca2+]i in PASMCs.