Aim To study the activity and mechanism of inhibition of myocardial hypertrophy of total fla-vonoids of Cydonia oblonga Mill. in spontaneously hy-pertensive rats ( SHR) . Methods Total flavonoids of COM ( COMF) were separated and purified by the op-timal process. SHR were divided into 6 groups: SHR control group ( SHR) , captopril group ( SHR+CAP, 25 μg·g-1 ) , Eucommia ulmoides Oliver group ( SHR+EUO, 30 μg·g-1 ) , low ( SHR+COMF-L, 40 μg ·g-1 ) , middle ( SHR+COMF-M, 80 μg·g-1 ) and high dose ( SHR+COMF-H, 160 μg·g-1 ) of COMF groups. Wistar-Kyoto (WKY) rats (n=8) were given distilled water as control. The drugs were given by in-tragastric administration for 16 weeks. The histological and pathological examinations of the heart were per-formed and organic damage was valued. The levels of AngⅡand ALD in blood and heart were evaluated. The mRNA and protein expression of ACE, ACE2 and AT1 was determined by RT-PCR and Western blot to e-valuate the effect of COMF on RAAS. Results Com-pared with SHR control group, HW, HW/BW, LVM and LVM/BW decreased in SHR+COMF-M and SHR+COMF-H groups. Cadiomyocyte hypertrophy was in-hibited in COMF groups. The concentration of AngⅡand ALD in heart and blood decreased. ACE and AT1 mRNA and protein expression in heart tissue de-creased, while ACE2 mRNA expression increased ( P<0. 01 or P <0. 05 ) , Conclusion Total flavonoids of Cydonia oblonga Mill. show the effect of inhibition of myocardial hypertrophy in spontaneously hyperten-sive rats and the mechanism is related to inhibiting ac-tivity of renin-angiotensin-aldosterone system.