On the other hand, antagonism of AT4R by divalinal completely abolished the protective effect of high-dose Ang IV, indicating the effect of Ang IV on diabetic cardiomyopathy was mediated essentially via AT4R. These results were consistent with a previous report that Ang IV treatment attenuated ischemia/reperfusion-induced cardiac injury, and this salutary effect was blunted by AT4R antagonist but not by AT1R, AT2R or MasR antagonists 14. This evidence concerns the gene MAS1L and diabetic cardiomyopathy.