Although there are many factors involved in the development of hypertensive MVR, such as a lack in tissue VEGF, an extracellular matrix more resistant to peptidases, a defect in VEGF receptors, an imbalance between Ang1 and Ang2, and so on, accumulating data demonstrated that EPC-related deficient angiogenesis contributes to MVR in hypertension. This evidence concerns the gene VEGFA and hypertensive disorder.