Although further elucidations regarding the signaling pathways involved in Mas activation are necessary, some mechanisms have been proposed. Overexpression of Ang-(1-7) in hearts of rats causes an improvement in the [Ca 2+ ] handling in cardiomyocytes and increases the expression of SERCA2a [21] . In keeping with these results, cardiomyocytes from Mas-deficient mice present slower [Ca 2+ ] i transients accompanied by a lower Ca 2+ ATPase expression in the sarcoplasmic reticulum [66, 76] . Although acute Ang-(1-7) treatment failed to alter Ca 2+ handling in ventricular myocytes of rats [76] , these findings suggest an important role of the Ang-(1-7)/Mas in the long-term maintenance of the Ca 2+ homeostasis in the heart.