Acacetin apparently normalized the abnormal mitochondrial morphology, protected against oxidative stress induced mitochondrial dysfunction by inhibiting the opening of mPTP, improved mitochondrial dynamics by regulating the balance between DRP1 and OPA1, inhibited excessive ROS generation-induced endothelial cell apoptosis and AKT/eNOS inactivation, and subsequently reversed the decreased endothelium-dependent dilation in hypertension. The gene discussed is OPA1; the disease is hypertensive disorder.