They further indicate that SGLT1 and SGLT2 protein levels are up-regulated ex vivo in pathological rat arteries (i.e., aortic arch, Ang II- and eNOS inhibitor-treated thoracic aorta vs. thoracic aorta) promoting oxidative stress in the arterial wall and endothelial dysfunction most likely subsequent to the impaired endothelial formation of NO. The gene discussed is SLC5A2; the disease is endothelial dysfunction.