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[目的]探讨JNK信号通路对缺氧诱导心房钠尿肽(ANP)分泌的影响及其机制.[方法]采用由氮气制作的家兔缺氧离体心房灌流模型;采用放射免疫法测定ANP及内皮素-1(ET-1)值.[结果]在家兔离体心房灌流模型中,急性缺氧明显促进心房ANP及ET-1的分泌;MAPK信号转导通路的JNK途径抑制剂SP600125明显抑制缺氧引起的ANP及ET-1的分泌;预处理SP600125或同时预处理2种ET-1受体阻断剂(BQ123+BQ788)均明显抑制缺氧诱导心房ANP的分泌,而SP600125对缺氧诱导ANP分泌的抑制作用明显强于BQ123+BQ788的抑制效应.[结论]急性缺氧明显增加离体心房ANP的分泌,JNK信号通路部分通过ET-1调节缺氧诱导ANP分泌的过程.
[Objective] To investigate the effect of JNK signal pathway on the secretion of atrial natriuretic peptide (ANP) induced by hypoxia and its mechanism. [Methods] Rabbit hypoxia isolated atrial perfusion model made by nitrogen was used to measure the ANP and (ET-1). [Results] Acute hypoxia significantly promoted the secretion of ANP and ET-1 in rabbit atrial ventricular perfusion model; SP600125, a MAPK signal transduction pathway inhibitor, was significantly Inhibition of ANP and ET-1 secretion induced by hypoxia; preconditioning of SP600125 or pretreatment of both ET-1 receptor blockers (BQ123 + BQ788) significantly inhibited hypoxia-induced atrial ANP secretion, while SP600125 The inhibitory effect of oxygen-induced ANP secretion was significantly stronger than that of BQ123 + BQ788. [Conclusion] Acute hypoxia can significantly increase the excretion of ANP in isolated atrial and JNK signaling pathway partly regulates the secretion of ANP through hypoxia.