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Updated: Apr 12, 2026
Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
Published on: June 29, 2014
ACE2-Ang (1-7) axis is induced in pressure overloaded rat model
Bai Liang1, Yongqin Li2, Zhenhua Han2
1Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China ; Research Institute of Atherosclerotic Disease, Xi'an Jiaotong University Cardiovascular Research Center Xi'an, Shaanxi, China ; Laboratory Animal Center, Xi'an Jiaotong University School of Medicine Xi'an, Shaanxi, China.
Abstract:
ACE2-Ang (1-7) axis is a key regulator in cardiac hypertrophy, myocardial remodeling and development of heart failure. To investigate how ACE2-Ang (1-7) axis function in pressure-overload-induced heart failure, male SD rats (weighing about 250 g) were used to establish the model of pressure-overload-induced heart failure using aortic stenosis surgery. The level of plasma ACE2, ACE and Ang (1-7) from heart failure group were significantly up-regulated compared with the sham group by ELISA test. The mRNA and protein expression of ACE2 in myocardial tissue from heart failure group also showed remarkably increased. Importantly, we found that the expression of ACE2 and Ang (1-7) were reversed in heart failure group after treatment with AT1 receptor antagonist telmisartan. Compared with heart failure group, the level of plasma ACE2, ACE and Ang (1-7) were significantly decreased in telmisartan treated group. The mRNA and protein expression of ACE2 in cardiac tissue from telmisartan group was also significantly decreased, while Mas mRNA and protein level was increased. Taken together, these studies demonstrated that the expression of ACE2-Ang (1-7) axis was induced in pressure-overload-induced heart failure model, suggesting that ACE2-Ang (1-7) axis may have a protective role in the development of heart failure and may provide a new target for drug development of heart failure.
