It has been shown that in response to fetal programming events (antenatal glucocorticoid exposure, low-protein diet in animal models, or preterm birth in humans) the activity of the protective ACE2-Ang(1–7)-MasR pathway is markedly reduced, and the classical ACE-AngII-AT1R pathway predominates that results in endothelial dysfunction with ROS generation, inflammation, sodium retention, blood pressure elevation, and tissue fibrosis [178]. Here, AGT is linked to endothelial dysfunction.