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EXP3174对交感神经损毁大鼠血管紧张素受体的调控

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摘要 目的阐明EXP3174调控AT1R的药理学特征及其活性对交感神经系统的依赖性。方法以6-OHDA化学切断法损毁大鼠交感神经,测定EXP3174干预后颈动脉血压及离体主动脉环张力对AngⅡ的反应性的变化。结果①6-OHDA化学切断法自幼年损毁大鼠交感神经,大鼠成年后收缩压(SBP)、舒张压(DBP)与心率(HR)对酪胺的反应性较之对照组明显减弱;②在整体动物,静脉注射EXP3174 0.1,0.2,0.4,0.8,1.6mg/kg,可减弱健全大鼠与交感神经损毁大鼠AngⅡ的升压效应,使AngⅡ升压反应的最大效应降低;在健全大鼠及交感神经损毁大鼠动脉环,EXP3174 0.1,0.3,1.0,3.2,10.0pmol.L-1预孵育均可减弱AngⅡ的缩血管反应,降低最大效应;③EXP3174在整体动物对AngⅡ升压效应的拮抗作用在交感神经损毁大鼠较健全大鼠下降,而体外血管环灌流实验的结果则显示在健全大鼠与交感神经大鼠药物作用无显著差异。结论EXP3174在体内除了直接作用于AT1R外,还可能与去甲肾上腺素的释放有关。
出处 《四川医学》 CAS 2005年第9期947-949,共3页 Sichuan Medical Journal
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