李倩, 张荣, 吕昌莲, 刘艳, 王珍, 朱大岭. Kv通道亚型在15-HETE收缩肺动脉过程中的作用J. 药学学报, 2006, 41(5): 412-417.
引用本文: 李倩, 张荣, 吕昌莲, 刘艳, 王珍, 朱大岭. Kv通道亚型在15-HETE收缩肺动脉过程中的作用J. 药学学报, 2006, 41(5): 412-417.
LI Qian, ZHANG Rong, Lü Chang-lian, LIU Yan, WANG Zhen, ZHU Da-ling. The role of subtypes of voltage-gated K+ channels in pulmonary vasoconstriction induced by 15-hydroeicosatetraenoic acidJ. Acta Pharmaceutica Sinica, 2006, 41(5): 412-417.
Citation: LI Qian, ZHANG Rong, Lü Chang-lian, LIU Yan, WANG Zhen, ZHU Da-ling. The role of subtypes of voltage-gated K+ channels in pulmonary vasoconstriction induced by 15-hydroeicosatetraenoic acidJ. Acta Pharmaceutica Sinica, 2006, 41(5): 412-417.

Kv通道亚型在15-HETE收缩肺动脉过程中的作用

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

  • 摘要: 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。

     

    Abstract: AimTo 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. MethodsIn the present study, ring of rabbit PA with specific KV 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 KV in PASMCs exposed to 15-HETE,chronic hypoxia. ResultsBlocking 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. ConclusionThe 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.

     

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