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.