Kv通道亚型在15-HETE收缩肺动脉过程中的作用

目的从组织功能及细胞分子水平研究电压门控型钾通道(Kv通道)亚型在15-羟化二十碳四烯酸(15-HETE)致大鼠肺动脉收缩过程中的作用。方法采用组织浴槽血管环法，使用Kv通道阻断剂，确定受15-HETE调控大鼠肺动脉平滑肌细胞(PASMCs)膜上Kv亚型；使用RT-PCR和Western blotting技术观察受15-HETE调控PASMCs 膜上Kv亚型。结果阻断Kv1.1，Kv1.2，Kv1.3和Kv1.6通道并不影响15-HETE诱导肺动脉血管收缩；15-HETE不影响PASMCs膜上Kv1.1和Kv1.2通道蛋白质表达；15-HETE下调PASMCs膜上Kv1.5和Kv2.1通道mRNA和蛋白质表达。结论缺氧可能是通过15-HETE这一介导因子抑制Kv1.5和Kv2.1通道，减少PASMCs膜上功能性Kv1.5和Kv2.1通道数量，导致PASMCs收缩。

The role of subtypes of voltage-gated K+ channels in pulmonary vasoconstriction induced by 15-hydroeicosatetraenoic acid

Aim To observe the effect of subtypes of Kv channels in rat pulmonary artery smooth muscle cells(PASMCs) on the process of pulmonary vasoconstriction induced by 15-HETE.Methods In the present study,ring of rabbit PA with specific K_(V) channel blockers were employed to functionally identify certain channel subtypes that took part in the process of 15-HETE induced pulmonary vasoconstriction;RT-PCR and Western blotting analysis were also used to measure the expression of subtypes of K_(V) in PASMCs exposed to 15-HETE,chronic hypoxia.Results Blocking of Kv1.1,Kv1.2,Kv1.3 and Kv1.6 channels did not affect 15-HETE induced vasoconstriction in normoxic rats;15-HETE did not affect expression of Kv1.1 and Kv1.2 channels;15-HETE significantly downregulated the expression of mRNA and protein of Kv1.5 and Kv2.1 in rat PASMCs. Conclusion The results suggested that hypoxia may block Kv1.5 and Kv2.1 channels via 15-HETE mediated mechanism,leading to decrease numbers of functional Kv1.5 and Kv2.1 channels in PASMCs,leading to PA vasoconstriction.