In summary, Ca2+ overload via the reverse mode of NCX1 and VDC, followed by ROS overproduction, p38 MAPK activation, and ET-1 overproduction, plays an important role in the contrast-induced renal hemodynamic disorder and renal tubular epithelial cell apoptosis, which suggests that, in clinical practice, CCB should be recommended to patients with hypertension who are undergoing radiographic examination or therapy requiring contrast media and that selective inhibitors of NCX1 may be beneficial in the prevention and treatment of CI-AKI in humans. This evidence concerns the gene EDN1 and hypertensive disorder.