Background; Angiotensin Type I receptor (AT1R) plays important role in regulation of cardiac function. Recent cellular studies shown that selective activation of 棺-arrestin-2 pathway of AT1R enhanced cardiac contractibility. However, in vivo study was not demonstrated. Methods; we investigated change of hemodynamic and cardiac function using selective 棺-arrestin-2 agonist of AT1R (TRV120023) in pressure volume loop (PVL) study. Results; 1. TRV120023 significantly decreased mean arterial pressure by dose dependant manner, which was arisen from blocking effect of G-protein pathway of AT1R. 2. In PVL study, TRV 120023 significantly increased cardiac contractibility-end systolic pressure volume relationship (ESPVR) and ejection fraction (EF) in wild type mice. However, losartan (棺-arrestin-2 pathway of AT1R blocker) significantly decreased ESPVR and EF in wild type mice. In 棺-arrestin 2 KO mice, TRV120023 significantly decreased ESPVR and EF by dose dependant manner. These findings indicated that improving of cardiac performance by TRV120023 is completely dependent on 棺-arrestin-2 pathway of AT1R. Conclusion; These data demonstrated that TRV120023 blocked G-protein pathway and resulted angiotensin II induced blood pressure elevation. Furthermore, TRV120023 stimulated 棺-arrestin-2 pathway of AT1R, which enhanced cardiac performance.