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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

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2010年第2期
页码:
161-163
栏目:
基础研究
出版日期:
2010-03-04

文章信息/Info

Title:
Expression of calcineurin inhibitor in myocardium in renovascular hypertensive rats
作者:
李朝晖; 谢晓华; 刘丽; 陈雯; 常连庆; 邓昭阳
解放军总医院南外一科, 北京 100853
Author(s):
LI Zhao-hui;  XIE Xiao-hua;  LIU Li;  CHEN Wen;  CHANG Lian-qing;  DENG Zhao-yang
Surgery Department, South Building, PLA General Hospital, Beijing 100853, China
关键词:
肾性高血压; 心肌组织; 钙调神经磷酸酶抑制因子; 大鼠
Keywords:
renovascular hypertension;  myocardium;  calcineurin inhibitor
分类号:
R544.14
DOI:
-
文献标识码:
A
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.

参考文献/References

［1］ Bueno OF, van Rooij E, Molkentin JD, et al. Calcineurin and hypertrophic heart disease: novel insights and remaining questions［J］. Cardiovascular Res, 2002, 53(4):806-821.

［2］ Takeda R, Suzuki E, Takahashi M, et al. Calcineurin is critical for sodium-induced neointimal formation in normotensive and hypertensive rats［J］. Am J Physiol Heart Circ Physiol, 2008, 294(6):H2871-H2878.

［3］ Sheng H, Zhu J, Wu X, et al. Angiotensin-converting enzyme inhibitor suppress activation of calcineurin in renovascular hypertensive rats［J］. Hypertens Res, 2007, 30(12):1247-1254.

［4］ Hill JA, Rothermel B, Yoo KD, et al. Targeted inhibition of calcineurin in pressure-overload cardiac hypertrophy［J］. J Biol Chem, 2002, 277(12):10251-10255.

［5］ Diedrichs H, Hagemeister J, Chi M, et al. Activation of the calcineurin/NFAT signaling cascade starts early in human hypertrophic myocardium［J］. J Int Med Res, 2007, 35(6):803-818.

［6］ Luedde M, Katus HA, Frey N. Novel molecular targets in the treatment of cardiac hypertrophy［J］. Recent Pat Cardiovasc Drug Discov, 2006, 1(1):1-20.

［7］ Frank D, Kuhn C, van Eickels M, et al. Calsarcin-1 protects against angiotensin-II induced cardiac hypertrophy［J］. Circulation, 2007, 116(22):2587-2596.

［8］ Faul C, Dhume A, Schecter AD, et al. Protein kinase A, Ca2+/calmodulin-dependent kinase II, and calcineurin regulate the intracellular trafficking of myopodin between Z-disc and the nucleus of cardiac myocytes［J］. Mol Cell Biol, 2007, 27(23):8215-8227.

［9］ Lemmens K, Segers VF, Demolder M, et al. Endogenous inhibitors of hypertrophy in concentric versus eccentric hypertrophy［J］. Eur J Heart Fail, 2007, 9(4):352-356.

备注/Memo

备注/Memo:
收稿日期：2009-3-12.基金项目：“十·五”军队重点基金资助(02Z0010)通讯作者：谢晓华，主任医师，主要从事心血管系统的围手术期治疗Email:n4xxh@126.com作者简介：李朝晖，副主任医师，硕士Email: lwzhxy@263.net
更新日期/Last Update: 2010-03-05