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急性缺氧抑制大鼠肺动脉平滑肌细胞钙ATP钾通道
http://www.100md.com 《中华结核和呼吸感染》 1998年第7期
离子通道|肺动脉|平滑肌细胞|缺氧症,关键词:
急性缺氧抑制大鼠肺动脉平滑肌细胞钙ATP钾通道
急性缺氧抑制大鼠肺动脉平滑肌细胞钙ATP钾通道

     肖欣荣 陈文彬 程德云 610041 成都,华西医科大学附属第一医院呼吸内科 中华结核和呼吸感染 1998 7 21 7


    关键词:离子通道;肺动脉;平滑肌细胞;缺氧症 期刊 zhjhhhxgr 0 论 著 fur -->


    

摘要 目的 研究急性缺氧对大鼠肺动脉平滑肌细胞钾通道活性的影响,以探讨钾通道活性改变在急性低氧性肺血管收缩(HPV)反应中所起的作用。方法 应用膜片钳单通道技术,在对称性高钾溶液中,于急性酶分离的大鼠单个肺动脉平滑肌细胞的内面向外式膜片 (inside-out patch)上,记录外向性钾通道电流,并用常氧和低氧的细胞浴液持续灌流肺动脉平滑肌细胞,以观察其对外向性钾通道电流的影响。结果 在记录的外向性钾电流中,证实了一种电流为钙、ATP激活性钾通道(K+ Ca-ATP );用低氧的细胞浴液灌流肺动脉平滑肌细胞可明显抑制这种钙、ATP激活性钾通道的活性(P<0.01)。而钾通道开放剂卡吗克啉(cromakalim)对低氧所抑制的肺动脉平滑肌细胞钙、ATP激活性钾通道具有明显的激活作用(P<0.01)。结论 急性低氧可通过对钙、ATP激活性钾通道的抑制作用,使肺动脉平滑肌细胞膜发生去极化,肺动脉收缩而导致急性肺血管阻力增加,进而产生肺动脉高压。肺动脉平滑肌细胞钙、ATP激活性钾通道活性的降低,可能在低氧性肺血管收缩反应中起着重要的作用。Cromakalim可作为拮抗低氧性肺血管收缩的有效药物之一。

The inhibitioneffect of acute hypoxia on K+ Ca-ATP channels of pulmonary arterysmooth muscle cells of rats

Xiao Xinrong, Chen Wenbin,Cheng Deyun. Respiratory Department, First Affiliated Hospital, West China University ofMedical Science, Chengdu 610041

Abstract Objective To explore the possible mechanism underlying hypoxic pulmonaryvasoconstriction, we evaluated the effect of acute hypoxia on potassium channels inpulmonary artery smooth muscle cells. Method The single smooth muscle cell was freshly isolated from pulmonaryartery (Φ700~200 μm) of Wistarrats with acute enzymatic digestion method. In symmertrical high K+ solution,we separated one outward K+ current from the patch of smooth muscle cells withinside-out configuration using patch-clamp technique. According to theelectrophysiological response to the patch channel, this current was identified as the Ca2+ ,ATP activated potassium channel (K+ Ca-ATP ). The hypoxic solution wasobtained by aeration with 5% CO2 -balance N2 mixurte. Result The currents of K+ Ca-ATP in thepatch of smooth muscle cells was much inhibited while the oxygen tension of solution wasreduced from normoxic (PO2 ≥13.33 kPa) to hypoxic (PO2 ≤2.67 kPa)levels (P<0.01). Cromakalim (10 nmol/L), an opener of potassium channel, could activatethe currents of K+ Ca-ATP decreased by acute hypoxia (P<0.01). Conclusion Acute hypoxia has an inhibition role on K+ Ca-ATP currents in pulmonary artery smooth muscle cells, causes the membrane potentionaldepolarization, leads to pulmonary vasoconstriction, increases pulmonary vascularresistence and artery pressure. The decrease of K+ Ca-ATP contributesto development of hypoxic pulmonary vasoconstriction. Cromakalim is one of effectiveantagonists for hypoxic pulmonary vasoconstriction.

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