15-HETE对肺动脉平滑肌细胞钙离子浓度的影响

目的　通过阻断细胞外钙离子 (Ca2+ )内流,观察 15 羟化二十烷四烯酸 ( 15 HETE)对兔肺动脉环收缩张力和肺动脉平滑肌细胞内游离钙浓度 ( Ca2+ ]i)的影响,探讨缺氧时 15 HETE引起细胞钙动员的机制。方法　采用组织浴槽血管环方法观察L 型钙通道阻断剂硝苯地平和无钙液对15 HETE诱导的兔肺动脉环收缩力的影响;酶法分离培养兔肺动脉平滑肌细胞,激光扫描共聚焦显微镜测定 15 HETE对细胞内 Ca2+ ]i的作用。结果　在正常组和缺氧组, 10μmol·L-1硝苯地平和无钙液对 1μmol·L-1 15 HETE引起的肺动脉环收缩均没有影响;培养的 15 HETE组细胞 (正常培养的细胞暴露于 1 μmol·L-1 15 HETE下继续孵育 8min)与正常对照组相比,细胞内 Ca2+ ]i明显增加 (P<0 05)。结论　15 HETE可引起肺动脉平滑肌细胞 Ca2+ ]i增加,且此钙来源于细胞内贮钙库的释放。

The effect of 15-HETE on the cytosolic [Ca2+]i in rabbit pulmonary artery smooth muscle cells(PASMC)

Aim The purpose of this study was to observe the eff ec t of 15-HETE on rabbit pulmonary artery(PA) vasoconstriction after removing ext racellular Ca 2 and on Ca 2 ] i in PASMCs and to discuss the mech anisms of cytosolic Ca 2 mobilization induced by 15-HETE.Methods We used tention studies of PA rings to observe the effect of L-type C a 2 channel blocker and non-Ca 2 solution on PA vasoconstriction induc ed by 15-HETE. Then we used laser-scanning confocal microscope to investigate Ca 2 ] i signaling in cultured PASMCs.Results L-type Ca 2 channel blocker and non-Ca 2 solution had no effect on 15-HET E induced vasoconstriction in normoxic and hypoxic rabbit PA rings. The increase of Ca 2 ] i was shown in 15-HETE group cells and the change in Ca 2 ] i induced by 15-HETE was significantly different from that of control. Conclusion 15-HETE may activate Ca 2 release from intrac ellular stores and raise Ca 2 ] i in PASMCs.