Further, deletion of AT1a receptors or NHE3 in the proximal tubules effectively block a key pathway in the development and sustenance of 2K1C hypertension, i.e., increased circulating and intratubular Ang II-stimulated proximal tubule Na+ reabsorption and induce salt retention by impairing the pressure-natriuresis response [32,33,34,35,59,60]. Here, AGT is linked to hypertensive disorder.