AimTo observe effect of angiotensin (1-7) (Ang-1-7) on myocardial hypertrophy in endoplasmic reticulum stress ( ERS ) induced cell injury.MethodsExperiment was divided into control group, angiotensin Ⅱ(AngⅡ) group, AngⅡ + Ang-1-7 group.Cultured rat myocardial cells were induced hypertrophy by different concentrations of AngⅡ (100 nmol / L, 1000 nmol / L) for 24, 48 and 72 hours, and intervened by different concentrations of Ang-1-7 (10 nmol/L, 100 nmol/L, 1000 nmol/L).After finishing experiment, the change of myocardial cells was observed in an inverted phase contrast microscope.Coomassie brilliant blue G-250 was used to determine cardiac total protein synthesis.Reverse transcription polymerase chain reaction (RT-PCR) and Western-Blotting were used to detect glucose-regulated protein 78(GRP78) and C/EBP homologous protein (CHOP) expression of endoplasmic reticulum stress(ERS).ResultsCompared with the control group, 100 nmol/L AngⅡ induced cardiac hypertrophy at 24 h, the myocardial cell volume increased, the cell protein content increased（1.59±0.03 g/L,p＜0.05）.mRNA and protein expression levels of endoplasmic reticulum stress proteins GRP78 and CHOP were significantly higher（p＜0.05）; Ang-1-7 can reverse the above to a large extent（p＜0.05）.ConclusionMyocardial hypertrophy induced by AngⅡ exist endoplasmic reticulum stress.Ang-1-7 can reduce the endoplasmic reticulum stress by reducing cardiac hypertrophy, and protect myocardial cells; Protective effect of 1000 nmol/L Ang-1-7 was the strongest.