Since the discovery of Ang-(1-7) in the late 1980s [63, 64] , several studies have demonstrated important effects of this peptide in hearts. The presence of Ang-(1-7) and its receptor Mas in the heart [65, 66] and the ability of this organ to produce Ang-(1-7) [55, 67] are evidences of the role of this peptide in cardiac tissues. Functionally, Ang-(1-7) induces an antiarrhythmogenic effect against ischemia/reperfusion injuries in rats [17, 68] as well as prevents atrial tachycardia and fibrillation in rats and dogs [69, 70] . Treatment with Ang-(1-7) improved the coronary perfusion and cardiac function in rats after myocardial infarction [71] and after ischemia/reperfusion injury [72] . Increases in circulating Ang-(1-7) levels in transgenic rats reduced the cardiac hypertrophy [17] and fibrosis [20, 22] induced by isoproterenol administration. These effects are apparently independent of changes in blood pressure since Grobe and colleagues [18] have demonstrated that the antifibrotic and antihypertrophic actions of Ang-(1-7) are still observed in Ang-II-infused hypertensive rats. Local overexpression of Ang-(1-7) in hearts of mice and rats improved the myocardial contractility and prevented the isoproterenol-and hypertension-induced cardiac remodeling [19, 21] . Altogether, these findings support a direct effect of Ang-(1-7) in the heart.