MAS1 and Ureteral obstruction: In this regard, while Pinheiro et al [16] showed that genetic deletion of Mas receptor in C57BL/6 mice led to glomerular hyperfiltration, proteinuria and renal fibrosis, Esteban et al [17] reported that renal deficiency for Mas diminished renal damage in unilateral ureteral obstruction and ischemia/reperfusion injury and the infusion of Ang-(1–7) to wild-type mice elicited inflammatory response.