Using both the mouse model of sunitinib cardiotoxicity and the in vitro H9c2 cardiomyocyte model of SU toxicity and SU-TMZ co-administration, we show that TMZ reverses SU-induced hypertension and left ventricular dysfunction (LVD) in mice, and alleviates SU-induced H9c2 cardiomyocyte viability loss via the AMPK/mTOR/autophagy pathway. This evidence concerns the gene MTOR and hypertensive disorder.