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作 者:叶红[1] 金肆[1] 叶仕桥[1] 邓世苇[1] 柯丹[1] 胡清华[1] 刘声远[1] 王迪浔[1]
机构地区:[1]华中科技大学同济医学院病理生理系卫生部呼吸系疾病重点实验室,湖北武汉430030
出 处:《中国病理生理杂志》2007年第2期262-265,共4页Chinese Journal of Pathophysiology
基 金:国家自然科学基金资助项目(No.39770309)
摘 要:目的:观察吸烟对大鼠肺动脉平滑肌大电导的钙激活的钾通道(BKCa)和电压依赖性延迟整流钾通道Kv1.5蛋白和mRNA表达的影响,以阐明吸烟引起的肺血管反应性改变中钾通道表达的变化。方法:复制大鼠的慢性吸烟模型,采用HE染色、免疫组织化学染色、原位杂交等方法。结果:(1)慢性吸烟可降低大鼠肺动脉平滑肌BKCa蛋白和mRNA表达;(2)慢性吸烟可降低大鼠肺动脉平滑肌Kv1.5蛋白和mRNA表达;(3)大动脉BKCa的降低程度大于Kv1.5,小动脉BKCa和Kv1.5的降低程度无明显差异。结论:慢性吸烟可下调大鼠肺动脉平滑肌钾通道BKCa和Kv1.5的表达水平,是导致肺血管反应性增高的机制之一。AIM : To investigate the role of potassium channel expression alteration in chronic cigarette smoking - induced increase in pulmonary vascular responsiveness, the effect of chronic cigarette smoking on large - conductance calcium- activated potassium channel (BKCa) and voltage- dependent delayed rectifier potassium channel (Kv1. 5 ) expression in rat pulmonary smooth muscle cells were investigated in vivo. METHODS: HE staining, immuno - histochemistry and in situ hybridization techniques were used. RESULTS: (1) Chronic cigarette smoking downregulates the protein and mRNA expression of BKc. in pulmonary arterial smooth muscles. (2) Chronic cigarette smoking downregulated the protein and mRNA expression of Kv1. 5 in pulmonary arterial smooth muscles. (3) In big artery, BKCa decreased more makedly than Kv1. 5, but in small artery, both of them decreased equally. CONCLUSION: Chronic cigarette smoking downregulates the levels of BKCa and Kv1. 5 in rat pulmonary arterial smooth muscle cells in vivo, which maybe contribute to the mechanism of cigarette smoking - induced increase in pulmonary vascular responsiveness.
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