卡托普利早期治疗自发性高血压大鼠抑制左室肥厚和c-myc表达而不影响c-fos表达(英文)  

Inhibition of left ventricular hypertrophy and expression of proto-oncogenes c-myc other than c-fos in myocardium by early captopril treatment in SHR rats

作　　者：陈松苍[1] 陈达光[1] 包幼迪[1] 晋学庆[1] 林应锵[1] 王华军[1] 

机构地区：[1]福建医学院附属第一医院高血压研究室

出　　处：《中国药理学报》1995年第3期217-222,共6页Acta Pharmacologica Sinica

基　　金：Supported by the National Natural Science Foundation of China, №3880409

摘　　要：目的:探讨早期卡托普利治疗抑制左室肥厚的机制.方法:♂SHR宫内期给药(100 mg·kg^(-1)·d^(-1))到16周,40周处死,测定收缩压,左室重与体重比,左室c-myc和c-fos表达量(Northern杂交).结果:治疗明显降低血压,停药后24周,仍维持较低血压(20.9±1.2vs对照SHR 28.3±1.3 kPa,P<0.01)并抑制左室肥厚,心肌c-myc表达明显减少(0.57±0.13 vs对照SHR 2.07±0.16,c-myc mRNA/18S rRNA,P<0.01),c-fos表达无变化.结论:卡托普利持久地阻止高血压形成,抑制左室肥厚.后者可能是抑制c-myc表达结果,治疗不改变c-fos表达.AIM:To explore the mechanisms by which angiotensin converting enzyme inhibitor (ACEI) prevents the development of left ventricular hypertrophy (LVH). METHODS: Captopril (Cap 100 mg.kg-1.d-1) was given orally to spontaneously hypertensive rats from intrauterine period to 16 wk of age. Ex-periments were performed at 40 wk of age. SBP, left ventricular weight to body weight ratio(LVW/BW) were assessed. The levels of c-myc and c-fos mRNA in the left ventricle were measured by Northern blot. RESULTS: Early-onset Cap therapy significantly decreased SBP. After discontinuance of treatment for 24 wk, SBP of SHRcap was still maintained at a lower level. LVW/BW in SHRcap was markedly reduced. The expression of myocardial c-myc mRNA was decreased by 72 % in SHRcap compared with that in the untreated SHR, but the expression of myocardial c-fos mRNA was not different between the untreated SHR, SHRcap,and WKY rats. CONCLUSION: Early Cap treatment may permanently prevent the development of hypertension, inhibit LVH. Furthermore, the prevention of LVH is associated with a decrease in c-myc mRNA levels, and the development and regression of left ventricular hypertrophy may be irrelevant to c-fos expression.

关 键 词：左心室肥厚 原癌基因蛋白 C-FOS 卡托普利 

分 类 号：R972[医药卫生—药品] R965.2[医药卫生—药学]