The evidence indicates that increased proximal tubular secretion AGT in humans and rodents with hypertension and diabetes [9,28,34,35] contribute to the intratubular augmentation of intratubular Ang II formation, as AGT spilled over the distal nephron serves as a substrate for prorenin filtered or produced by the collecting duct, which increases sodium reabsorption and blood pressure [2]. This evidence concerns the gene AGT and hypertensive disorder.