However, this was not the focus of the present study in that we specifically tested the hypothesis for the 1st time that deletion of AT1a receptors or its downstream target NHE3 alone selectively in the proximal tubules of the kidney was enough to attenuate or prevent the development of 2K1C Goldblatt hypertension, thus providing the new evidence for a critical role of proximal tubule AT1a receptors and NHE3 in the pathogenesis of 2K1C hypertension. Here, SLC9A3 is linked to Hypertension.