Effect of thyroid hormone on cardiac function on ischemia-reperfusion model: role of angiotensin type 2 receptor and AMPK signaling pathway

• Grant number: 12/15420-2
• Support Opportunities: Regular Research Grants
• Start date: November 01, 2012
• End date: October 31, 2014
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Maria Luiza de Morais Barreto de Chaves
• Grantee: Maria Luiza de Morais Barreto de Chaves
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Several endocrine systems, such as the renin-angiotensin system (RAS) and thyroid hormones (TH) alter the cardiac function, directly or indirectly modulating the heart trophism and protecting against cardiac stress. Besides their regulatory role under situations of cardiac damage, the endocrine systems are able to interact in many of their actions. The TH promote a phenotype of cardioprotection and influence the trophic state of cardiac tissue through numerous mechanisms, including the modulation of RAS components - the angiotensin II (Ang II), a potent vasoactive peptide and its receptors (AT1 and AT2). Previous studies have shown that changes in AT2 receptor expression in the myocardium are closely related to the functional response of the heart following ischemia/reperfusion (I/R) injury, and that its expression is increased by 50% in hyperthyroidism condition. This study aimed to evaluate the role of AT2 receptor in cardioprotection mediated by the TH and the involvement of AMP-activated protein kinase (AMPK), enzyme related to metabolism and cardioprotection, in this context. (AU)