首页|钙调神经磷酸酶抑制因子在肾性高血压大鼠心肌肥厚的信号转导

钙调神经磷酸酶抑制因子在肾性高血压大鼠心肌肥厚的信号转导

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目的:探讨一肾一夹肾性高血压大鼠模型中,心肌组织钙调神经磷酸酶(CaN)抑制因子(Cain)表达及血浆相关活性因子的变化.方法:健康雄性Wistar大鼠,随机分为3组(n=7),①假手术组;②手术组:通过一肾一夹法复制肾性高血压大鼠;③环孢素A(CsA)组:CsA 5 mg/(kg·d)皮下注射;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)及全心质量(HW)与体质量(BW)的比值,通过放免方法测定血浆醛固酮(Ald)及血管紧张素Ⅱ(AngⅡ)含量,运用蛋白印记杂交的方法,测定心肌组织Cain表达的变化.结果:手术组与假手术组比较,LVW/BW及HW/BW显著增加,血浆Ald和AngⅡ水平明显增加,CaN活性增加,Cain的表达显著增加(P<0.05);而CsA组与手术组比较,LVW/BW及HW/BW下降,血浆Ang Ⅱ和Ald水平显著下降,CaN活性减低,Cain的表达显著减少(P<0.05).结论:一肾一夹手术可以诱导大鼠血浆Ald和AngⅡ水平增加,通过CaN依赖的信号转导通路,诱导心肌肥厚反应的发生.同时,机体内源性Cain的表达的变化,受到CaN信号转导系统调控.
Signal pathway of calcineurin-inhibitor in cardiac hypertrophy of renovascular hypertensive rats
AIM:To investigate the signal pathway of myocardial calcineurin inhibitor (Cain) in renohypertensive rats treated with 1-kidney-1-clamp (1k1c) operation and to study the changes of related active factors in plasma. METHODS: Twenty-one male Wistar rats were randomly divided into 3 groups ( n = 7) : sham operatinggroup,operating group treated with 1k1c operation and cyclosporin A ( CgA) group treated with CsA 5 mg/( kg· d) after the 1k1c operation. Fourteen days after the treatment,AngⅡ and Ald levels in plasma were determined by radioimmunoassay and the expression of Cain in myocardium was determined by Western Blot. RESULTS: The Ald and AngⅡ levels,the expression of Cain and the activity of calcineurin in myocardium increased in operating group compared with those in sham operating group while the Ald and Ang Ⅱ levels,the expression of myocardial Cain and the activity of calcineurin significantly decreased in CsA group compared with those in operating group. CONCLUSION: The 1k1c operation induces cardiac hypertrophy through a calci-neurin-depedent signal pathway. The expression of internal Cain may be controlled by the activity of calcineurin.

calcineurin-inhibitorhypertension,renalcardiomyopathy,hypertrophic

李朝晖、谢晓华、刘丽、陈雯、常连庆、邓昭阳

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解放军总医院南外一科,北京,100853

钙调神经磷酸酶抑制因子 高血压,肾性 心肌病,肥厚性

军队重点课题

02Z0010

2009

第四军医大学学报
第四军医大学

第四军医大学学报

CSTPCDCSCD北大核心
影响因子:0.599
ISSN:1000-2790
年,卷(期):2009.30(12)
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