Since proximal tubule-specific deletion of AT1a, NHE3, or SIRT3 decreases basal blood pressure, and attenuates or augments Ang II-induced hypertension, we conclude that intratubular Ang II via AT1a, NHE3, or SIRT3 in the proximal tubules plays an important role in maintaining basal blood pressure and the development of hypertension and kidney injury. Here, AGT is linked to hypertensive disorder.