Collectively, our results suggest that chronic RAAS activation in (mREN2)27 HTN promotes (1) enhanced cardiac contractility through AngII-mediated AT1R stimulation and a compromised protective arm of AngII involving MAS1 and AT2 receptors and (2) disrupted calcium homeostasis due to increased NCX activity and decreased SERCA2 activity. This evidence concerns the gene ATP2A2 and hypertensive disorder.