Abstract: AIM: To observe the effect of the β1-receptor blocker,atenolol,on transverse aortic constriction(AAC)-induced myocardial hypertrophy.METHODS: Twenty-four male C57BL mice were randomly divided into four groups: normal control group,sham group,AAC operation group and AAC plus atenolol treatment group.After 4 weeks of treatment,echocardiogram was performed to assess cardiac function changes,heart weight to body weight ratio(HW/BW),heart weight/tibial length,left ventricular ejection fraction(LVEF%) and LV fractional shortening(FS%).Expression levels of ANP,BNP and β-MHC mRNAs in heart tissues and the size of cardiomyocytes were also measured using PCR and pathological techniques.RESULTS: Compared with those in AAC group,LVEDd decreased 24.9%,17.7% and 18.2% and LVEDs decreased 32.9%,34.1% and 26.3%,respectively,in normal control group,sham group and atenolol group,whereas EF increased 65.6%,75.8% and 49.5% and FS increased 79.7%,100.0% and 62.6%,respectively(P<0.05).LVM/BW and cardiac myocyte cross-sectional area showed a decrease in atenolol group compared with that in AAC group(P<0.01),but they still increased significantly compared with those in the normal control group.Expressions of ANP,BNP and α-MHC mRNAs in atenolol group were lower than those in AAC group(P<0.05).CONCLUSION: Atenolol can intervene during the progress of pressure overload-induced myocardial hypertrophy in C57BL mice.