Objective   To determine the effect of angiotensin(1-7) [Ang(1-7)] on the left ventricular hypertrophy and myocardial fibrosis in a pressure-overload hypertensive models

infra-nephric aorta coarctation (INAC)

and a renin-angiotensin-aldosterone system (RAAS) activation hypertensive model

two kidney one clip (2K1C) in the early and late stage.    Methods   Totally 120 health male Wistar rats were randomly and equally divided into 6 groups

that is

sham INAC group

INAC group

INAC Ang(1-7) group

sham 2K1C group

2K1C group and 2K1C Ang(1-7) group. INAC and 2K1C hypertensive models was established to corresponding groups and osmotic minipump implantation was carried out to the rats to deliver the Ang(1-7) to their body homogenously and to examine the parameters representing the blood pressure

including left ventricular hypertrophy (LVW

LVI

CA) and myocardial fibrosis (CVF and PVCA).    Results   Left ventricular hypertrophy (LVH) was observed in the early stage and developed in the late stage both in the 2K1C and INAC groups. Ang(1-7) decreased LVW

LVI

CA both in the early and late stage in the 2K1C model（P0.05）. But to INAC model

Ang (1-7) only decreased the pressures in the early stage（P0.05）

but not in the late stage（P0.05）. Myocardial fibrosis happened and developed progressively in the 2K1C hypertensive model（P0.05）. Ang(1-7) was able to alleviate interstitial as well as perivascular fibrosis as used in the early stage（P0.05）

while it only alleviated perivascular fibrosis in the late stage（P0.05）

had no marked effect on the interstitial fibrosis（P0.05）. There was a mild myocardial fibrosis happened in the left ventricle of the INAC model in the late stage（P0.05）

and Ang(1-7) was able to alleviate both interstitial and perivascular fibrosis effectively（P0.05）.    Conclusion   Ang(1-7) can effectively prevent and improve  left ventricular hypertrophy and myocardial fibrosis

but in the different stage

it exerts different effect

which indicate there are multiple mechanisms of Ang(1-7).