In previous work, we demonstrated that in the endothelium BPA could activate vasoregulatory genes such as angiotensin II and calcium-calmodulin kinase II responsible for endothelial dysfunction and hypertension, through a mechanism involving the uncoupling of endothelial nitric oxide synthase promoting a decreased of NO production and overproduction of oxygen free radicals42. This evidence concerns the gene NOS3 and hypertensive disorder.