卡托普利抑制自发性高血压大鼠左心室肥厚机制的研究

为了探讨血管紧张素转换酶抑制阻止左心室厚机制，对雄性自发性高血压大鼠从宫内期起给予卡托普利治疗，到１６周龄时停药，以年龄、性别配对的ＳＨＲ以及ＷＫＹ大鼠作对照，各组到４０周龄处死。

Investigation of the mechanism for inhibition of leftventricular bypertrophy by captopril treatment inspontaneously hypertensive rats

o explore the rnechanisms by which angiotensinconverting enzyme inhibrtor (ACEI) prevents the development of left ventricular hypertrophy (LVH) . capto-pril (Cap 100mg . kg-1 /d was administered orally tomale spontaneously hypertensive rats from intrauterineperiod to 16 weeks of age. Male and agematched un-treated WKY rats and SHR were used as controls. Ex-periments were performed at 40 weeks of age. SBP, leftventricular weight to body weight ratio (LVW/BW) ,myocardial hydroxyproline (Hypro) and norepinephrine(NE) were deterrnined. The levels of c-mvc and c-fosmRNA in the left ventricle were measured bv Northernblot. Early-onset Cap therapy significantly decreasedSBP at 16 weeks of age. After discontinuance of treat-ment for 24 weeks, SBP of SHRcap was still maintainedat a level lower than that of untreated SHR. LVW/BWand Hypro in SHR cap were markedly reduced. The ex-pression of myocardial cmyc mRNA (n= 5) was de-creased by 72% in SHRcap compared with that in theuntreated SHR, but the expression of cfos mRNA(n= 7) and NE was not different between the untreatedSHR, SHRcap and WKY rats. These resuhs indicatethat early Cap treatment may permanently prevent thedevelopment of hypertension, inhibit myocardial hyper-trophy (MH) , and interstitial fibrosis. Furthermore,the prevention of MH is associated with a decrease inmyocardial c-myc mRNA levels, and the developmentand regression of MH may be irrelevant to proto-onco-gene c-fos expression.