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The effects of different angiotensin II type 1 receptor blockers on the regulation of the ACE-AngII-AT1 and ACE2-Ang(1-7)-Mas axes in pressure overload-induced cardiac remodeling in male mice.
J Mol Cell Cardiol. 2016 08; 97:180-90.JM

Abstract

Angiotensin II (AngII) type 1 receptor blockers (ARBs) have been effectively used in hypertension and cardiac remodeling. However, the differences among them are still unclear. We designed this study to examine and compare the effects of several ARBs widely used in clinics, including Olmesartan, Candesartan, Telmisartan, Losartan, Valsartan and Irbesartan, on the ACE-AngII-AT1 axis and the ACE2-Ang(1-7)-Mas axis during the development of cardiac remodeling after pressure overload. Although all of the six ARBs, attenuated the development of cardiac hypertrophy and heart failure induced by transverse aortic constriction (TAC) for 2 or 4weeks in the wild-type mice evaluated by echocardiography and hemodynamic measurements, the degree of attenuation by Olmesartan, Candesartan and Losartan tended to be larger than that of the other three drugs tested. Additionally, the degree of downregulation of the ACE-AngII-AT1 axis and upregulation of the ACE2-Ang(1-7)-Mas axis was higher in response to Olmesartan, Candesartan and Losartan administration in vivo and in vitro. Moreover, in angiotensinogen-knockdown mice, TAC-induced cardiac hypertrophy and heart failure were inhibited by Olmesartan, Candesartan and Losartan but not by Telmisartan, Valsartan and Irbesartan administration. Furthermore, only Olmesartan and Candesartan could downregulate the ACE-AngII-AT1 axis and upregulate the ACE2-Ang(1-7)-Mas axis in vitro. Our data suggest that Olmesartan, Candesartan and Losartan could effectively inhibit pressure overload-induced cardiac remodeling even when with knockdown of Ang II, possibly through upregulation of the expression of the ACE2-Ang(1-7)-Mas axis and downregulation of the expression of the ACE-AngII-AT1 axis. In contrast, Telmisartan, Valsartan and Irbesartan only played a role in the presence of AngII, and Losartan had no effect in the presence of AngII in vitro.

Authors+Show Affiliations

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.Institute of Biomedical Sciences, Fudan University, Shanghai 200032, People's Republic of China.Institute of Biomedical Sciences, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China.Institute of Biomedical Sciences, Fudan University, Shanghai 200032, People's Republic of China.Institute of Biomedical Sciences, Fudan University, Shanghai 200032, People's Republic of China.Institute of Biomedical Sciences, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China; Institute of Biomedical Sciences, Fudan University, Shanghai 200032, People's Republic of China.Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, People's Republic of China; Institute of Biomedical Sciences, Fudan University, Shanghai 200032, People's Republic of China. Electronic address: zou.yunzeng@zs-hospital.sh.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27210827

Citation

Wang, Xingxu, et al. "The Effects of Different Angiotensin II Type 1 Receptor Blockers On the Regulation of the ACE-AngII-AT1 and ACE2-Ang(1-7)-Mas Axes in Pressure Overload-induced Cardiac Remodeling in Male Mice." Journal of Molecular and Cellular Cardiology, vol. 97, 2016, pp. 180-90.
Wang X, Ye Y, Gong H, et al. The effects of different angiotensin II type 1 receptor blockers on the regulation of the ACE-AngII-AT1 and ACE2-Ang(1-7)-Mas axes in pressure overload-induced cardiac remodeling in male mice. J Mol Cell Cardiol. 2016;97:180-90.
Wang, X., Ye, Y., Gong, H., Wu, J., Yuan, J., Wang, S., Yin, P., Ding, Z., Kang, L., Jiang, Q., Zhang, W., Li, Y., Ge, J., & Zou, Y. (2016). The effects of different angiotensin II type 1 receptor blockers on the regulation of the ACE-AngII-AT1 and ACE2-Ang(1-7)-Mas axes in pressure overload-induced cardiac remodeling in male mice. Journal of Molecular and Cellular Cardiology, 97, 180-90. https://doi.org/10.1016/j.yjmcc.2016.05.012
Wang X, et al. The Effects of Different Angiotensin II Type 1 Receptor Blockers On the Regulation of the ACE-AngII-AT1 and ACE2-Ang(1-7)-Mas Axes in Pressure Overload-induced Cardiac Remodeling in Male Mice. J Mol Cell Cardiol. 2016;97:180-90. PubMed PMID: 27210827.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The effects of different angiotensin II type 1 receptor blockers on the regulation of the ACE-AngII-AT1 and ACE2-Ang(1-7)-Mas axes in pressure overload-induced cardiac remodeling in male mice. AU - Wang,Xingxu, AU - Ye,Yong, AU - Gong,Hui, AU - Wu,Jian, AU - Yuan,Jie, AU - Wang,Shijun, AU - Yin,Peipei, AU - Ding,Zhiwen, AU - Kang,Le, AU - Jiang,Qiu, AU - Zhang,Weijing, AU - Li,Yang, AU - Ge,Junbo, AU - Zou,Yunzeng, Y1 - 2016/05/19/ PY - 2015/12/01/received PY - 2016/05/18/revised PY - 2016/05/18/accepted PY - 2016/5/24/entrez PY - 2016/5/24/pubmed PY - 2017/6/1/medline KW - Angiotensin II type 1-receptor blockers KW - Cardiac hypertrophy KW - Heart failure KW - Mechanical stretch KW - Pressure overload SP - 180 EP - 90 JF - Journal of molecular and cellular cardiology JO - J Mol Cell Cardiol VL - 97 N2 - Angiotensin II (AngII) type 1 receptor blockers (ARBs) have been effectively used in hypertension and cardiac remodeling. However, the differences among them are still unclear. We designed this study to examine and compare the effects of several ARBs widely used in clinics, including Olmesartan, Candesartan, Telmisartan, Losartan, Valsartan and Irbesartan, on the ACE-AngII-AT1 axis and the ACE2-Ang(1-7)-Mas axis during the development of cardiac remodeling after pressure overload. Although all of the six ARBs, attenuated the development of cardiac hypertrophy and heart failure induced by transverse aortic constriction (TAC) for 2 or 4weeks in the wild-type mice evaluated by echocardiography and hemodynamic measurements, the degree of attenuation by Olmesartan, Candesartan and Losartan tended to be larger than that of the other three drugs tested. Additionally, the degree of downregulation of the ACE-AngII-AT1 axis and upregulation of the ACE2-Ang(1-7)-Mas axis was higher in response to Olmesartan, Candesartan and Losartan administration in vivo and in vitro. Moreover, in angiotensinogen-knockdown mice, TAC-induced cardiac hypertrophy and heart failure were inhibited by Olmesartan, Candesartan and Losartan but not by Telmisartan, Valsartan and Irbesartan administration. Furthermore, only Olmesartan and Candesartan could downregulate the ACE-AngII-AT1 axis and upregulate the ACE2-Ang(1-7)-Mas axis in vitro. Our data suggest that Olmesartan, Candesartan and Losartan could effectively inhibit pressure overload-induced cardiac remodeling even when with knockdown of Ang II, possibly through upregulation of the expression of the ACE2-Ang(1-7)-Mas axis and downregulation of the expression of the ACE-AngII-AT1 axis. In contrast, Telmisartan, Valsartan and Irbesartan only played a role in the presence of AngII, and Losartan had no effect in the presence of AngII in vitro. SN - 1095-8584 UR - https://www.unboundmedicine.com/medline/citation/27210827/The_effects_of_different_angiotensin_II_type_1_receptor_blockers_on_the_regulation_of_the_ACE_AngII_AT1_and_ACE2_Ang_1_7__Mas_axes_in_pressure_overload_induced_cardiac_remodeling_in_male_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(16)30144-4 DB - PRIME DP - Unbound Medicine ER -