Gabriela P Diniz1, Nathalia Senger1, Marcela S Carneiro-Ramos2, Robson A S Santos3, Maria Luiza M Barreto-Chaves4. 1. Department of Anatomy, Laboratory of Cell Biology and Functional Anatomy, University of São Paulo, Sao Paulo, Brazil. 2. Human and Natural Sciences Center, Federal University of ABC, São Paulo, Brazil. 3. Department of Physiology and Biophysics, Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, BrazilCardiology Institute of Rio Grande do Sul, University Foundation of Cardiology. 4. Laboratory of Cellular Biology and Functional Anatomy, Department of Anatomy, Biomedical Sciences Institute, University of São Paulo, Av. Prof. Lineu Prestes 2415, Cidade Universitária, São Paulo, SP 05508-900, Brazil mchaves@usp.br.
Abstract
OBJECTIVES: Thyroid hormone (TH) promotes marked effects on the cardiovascular system, including the development of cardiac hypertrophy. Some studies have demonstrated that the renin-angiotensin system (RAS) is a key mediator of the cardiac growth in response to elevated TH levels. Although some of the main RAS components are changed in cardiac tissue on hyperthyroid state, the potential modulation of the counter regulatory components of the RAS, such as angiotensin-converting enzyme type 2 (ACE2), angiotensin 1-7 (Ang 1-7) levels and Mas receptor induced by hyperthyroidism is unknown. The aim of this study was to investigate the effect of hyperthyroidism on cardiac Ang 1-7, ACE2 and Mas receptor levels. METHODS: Hyperthyroidism was induced in Wistar rats by daily intraperitoneal injections of T4 for 14 days. RESULTS: Although plasma Ang 1-7 levels were unchanged by hyperthyroidism, cardiac Ang 1-7 levels were increased in TH-induced cardiac hypertrophy. ACE2 enzymatic activity was significantly increased in hearts from hyperthyroid animals, which may be contributing to the higher Ang 1-7 levels observed in the T4 group. Furthermore, elevated cardiac levels of Ang 1-7 levels were accompanied by increased Mas receptor protein levels. CONCLUSION: The counter-regulatory components of the RAS are activated in hyperthyroidism and may be contributing to modulate the cardiac hypertrophy in response to TH.
OBJECTIVES: Thyroid hormone (TH) promotes marked effects on the cardiovascular system, including the development of cardiac hypertrophy. Some studies have demonstrated that the renin-angiotensin system (RAS) is a key mediator of the cardiac growth in response to elevated TH levels. Although some of the main RAS components are changed in cardiac tissue on hyperthyroid state, the potential modulation of the counter regulatory components of the RAS, such as angiotensin-converting enzyme type 2 (ACE2), angiotensin 1-7 (Ang 1-7) levels and Mas receptor induced by hyperthyroidism is unknown. The aim of this study was to investigate the effect of hyperthyroidism on cardiac Ang 1-7, ACE2 and Mas receptor levels. METHODS:Hyperthyroidism was induced in Wistar rats by daily intraperitoneal injections of T4 for 14 days. RESULTS: Although plasma Ang 1-7 levels were unchanged by hyperthyroidism, cardiac Ang 1-7 levels were increased in TH-induced cardiac hypertrophy. ACE2 enzymatic activity was significantly increased in hearts from hyperthyroid animals, which may be contributing to the higher Ang 1-7 levels observed in the T4 group. Furthermore, elevated cardiac levels of Ang 1-7 levels were accompanied by increased Mas receptor protein levels. CONCLUSION: The counter-regulatory components of the RAS are activated in hyperthyroidism and may be contributing to modulate the cardiac hypertrophy in response to TH.
Authors: JiuChang Zhong; Ratnadeep Basu; Danny Guo; Fung L Chow; Simon Byrns; Manfred Schuster; Hans Loibner; Xiu-hua Wang; Josef M Penninger; Zamaneh Kassiri; Gavin Y Oudit Journal: Circulation Date: 2010-08-02 Impact factor: 29.690
Authors: Evi Kostenis; Graeme Milligan; Arthur Christopoulos; Carlos F Sanchez-Ferrer; Silvia Heringer-Walther; Patrick M Sexton; Florian Gembardt; Elaine Kellett; Lene Martini; Patrick Vanderheyden; Heinz-Peter Schultheiss; Thomas Walther Journal: Circulation Date: 2005-04-04 Impact factor: 29.690
Authors: Jennifer Lo; Vaibhav B Patel; Zuocheng Wang; Jody Levasseur; Susan Kaufman; Josef M Penninger; Gavin Y Oudit Journal: Exp Physiol Date: 2012-06-29 Impact factor: 2.969