李朝晖, 谢晓华, 刘丽, 陈雯, 常连庆, 邓昭阳. 血管紧张素Ⅱ-醛固酮诱导肾性高血压大鼠心肌肥厚发生:钙调神经磷酸酶抑制因子的作用[J]. 心脏杂志, 2010, 22(2): 161-163.
    引用本文: 李朝晖, 谢晓华, 刘丽, 陈雯, 常连庆, 邓昭阳. 血管紧张素Ⅱ-醛固酮诱导肾性高血压大鼠心肌肥厚发生:钙调神经磷酸酶抑制因子的作用[J]. 心脏杂志, 2010, 22(2): 161-163.
    Expression of calcineurin inhibitor in myocardium in renovascular hypertensive rats[J]. Chinese Heart Journal, 2010, 22(2): 161-163.
    Citation: Expression of calcineurin inhibitor in myocardium in renovascular hypertensive rats[J]. Chinese Heart Journal, 2010, 22(2): 161-163.

    血管紧张素Ⅱ-醛固酮诱导肾性高血压大鼠心肌肥厚发生:钙调神经磷酸酶抑制因子的作用

    Expression of calcineurin inhibitor in myocardium in renovascular hypertensive rats

    • 摘要: 目的: 探讨一肾一夹肾性高血压大鼠模型中,心肌组织中钙调神经磷酸酶(CaN)抑制因子(calcineurin-inhibitor,Cain)表达的变化,以及血浆中相关活性因子的变化。方法: 将21只健康雄性Wistar大鼠,随机分为3组(n=7),即假手术组、手术组(通过一肾一夹法复制肾性高血压大鼠)及螺内酯组:以螺内酯20 mg/(kg·d)灌胃;实验14 d后,大鼠称质量后抽血处死,分别计算左心室质量(LVW)、全心质量(HW)以及二者与体质量(BW)的比值。采用放射免疫测定法检测血浆醛固酮(Ald)及血管紧张素Ⅱ(AngⅡ)的含量。以蛋白印迹杂交的方法,测定心肌组织中Cain表达的变化。结果: 与假手术组比较,手术组大鼠的LVW/BW及HW/BW比值显著增加(P<0.05)、血浆Ald和AngⅡ的水平、及Cain的表达的显著增加(P<0.01);而与手术组比较,螺内酯组大鼠的LVW/BW比值显著减少(P<0.05)、血浆AngⅡ的水平及Cain的表达均显著减少(P<0.01)。结论: 通过一肾一夹手术,诱导机体内源性Ald和AngⅡ增加,导致大鼠心肌肥厚反应的发生。同时,机体内源性Cain表达的增加,以抑制CaN信号通路介导的心肌肥厚反应。螺内酯通过阻断Ald与其受体结合,可以抑制心肌肥厚的发生。

       

      Abstract: AIM: To investigate the expression of myocardial calcineurin inhibitor (Cain) in renal hypertensive rats and the changes of active related factors in plasma. METHODS: Twenty one male Wistar rats were randomly divided into three groups (n=7): sham operation group, operation group treated with traditional one kidney and one clamp operation, and spironolactone group treated with spironolactone [20 mg/(kg·day)]. Angiotensin II (AngII) and Ald levels in plasma were determined by radioimmunoassay. The expression of Cain in myocardium was determined by Western blot. RESULTS: Ald and AngII levels, expression of Cain and activity of calcineurin in myocardium all increased in operation group compared with those in sham operation group. AngII level markedly decreased in spironolactone group compared with that in the operation group. Expression of myocardial Cain level and calcineurin activity also decreased significantly. CONCLUSION: Internal Ald induces cardiac hypertrophy through a calcineurin-dependent signal pathway. The expression of internal Cain may be controlled by the activity of calcineurin.

       

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