High levels of thyroid hormones (TH) are responsible for promoting changes in the cardiovascular system, which culminate in the development of cardiac arrhythmias and the installation of a hypertrophic process (Cappola et al., 2006). We have previously demonstrated that TH is able to promote cardiac hypertrophy and other cardiovascular manifestations through Renin-Angiotensin-System (RAS), especially due to the action of the peptide angiotensin II (Ang II), since the inhibition of its action blunted TH-induced cardiovascular changes. On the other hand, Angiotensin (1-7) (Ang 1-7), a peptide synthesized by RAS, promotes antiarrhythmic and anti-hypertrophic effects, and corresponds to an important regulatory arm in RAS. Thus, the aim of this study is to verify if Ang 1-7 may influence the cardiovascular effects induced by thyroid hormones, which are commonly observed in hyperthyroid patients. To perform that, male Wistar rats will receive daily intraperitoneal injections of T3 (20x physiological dose) for 21 and 28 days. Simultaneously, part of the animals will receive continuous infusion of Ang 1-7 (24¼g/Kg/hr) during the same experimental period. Morphological and funcional analyses of the heart, as well as the expression of proteins related to cardiac remodeling and RAS components will, be evaluated in hearts of animals of different groups.
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