The renin-angiotensin system (RAS) is a key regulator of blood pressure (BP), with angiotensin II (ang II) acting as a major effector molecule via its receptors which are broadly expressed in a variety of tissues. Previous and ongoing work from our lab has demonstrated the significance of the type 1 angiotensin receptor in the kidney for BP homeostasis. We have taken the approach of gene-targeting in mice to study the role of the AT1A receptor in BP regulation and hypertension pathogenesis. Mice completely deficient in AT1A receptors had profound reductions (>20 mm Hg) in systolic blood pressure. Following this, we next used a kidney cross-transplantation approach to identify the kidney as a tissue with a distinct role in BP regulation by the RAS. Kidney AT1A KO mice had lower baseline BPs and were resistant to angiotensin II hypertension. Our more recent studies have investigated the function of the AT1A receptor in BP control in individual cell lineages in order to dissect the role of the RAS in specific regions of the kidney. To accomplish this, we utilized a cre-loxp approach for cell-specific gene targeting using a mouse line we generated with a conditional Agtr1a allele. We have systematically examined the role of the AT1A receptor in BP regulation in the renal proximal tubule, distal nephron and renal vasculature. Our studies have identified critical segments in the kidney for baseline blood pressure homeostasis, salt sensitivity, and regulation of hypertension. Together, our data suggest that type 1 angiotensin receptors in the kidney play a complex role in the integrated control of blood pressure.