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Tavares, FM. Effect of Thyroid Hormone on cardiac function in the Ischemia/Reperfusion injury of Wistar rats. Role of AT2 receptor and AMPK signaling pathway. Master thesis (Morphological Sciences) Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, 2012. Several endocrine systems, such as the renin-angiotensin system (RAS) and thyroid hormones (TH), may direct influence the cardiac function, directly or indirectly modulating the heart trophism and protectingagainst 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 correspond to 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. A model of I/R was developed in isolated hearts of Wistar rats submitted to T3 treatment (7μg/100g b.w. for 14 days) in the presence or absence of the AT2 receptor antagonist (PD123319), using the Langendorff apparatus. The results showed that TH exerts a cardioprotective effect accompanied by increased levels of AT2 and phosphorylated AMP protein expression. This increase was prevented by the administration of PD, which was accompanied by a loss of cardiac function. These data suggest that part of the TH-induced cardioprotection is mediated by the AT2 receptor with the involvement of AMPK in the protection of myocardium after I/R injury.

Efeito do hormônio tiroideano na função cardíaca no modelo de isquemia/reperfusão em ratos. Papel do receptor AT2 e da via intracelular AMPK.