The renal tubule transporters responsible for Na⁺ and water transport along the nephron have been identified and cloned, permitting comprehensive analysis of transporter protein abundance changes in complex physiological models by using a “targeted proteomics” approach. Here, we apply this approach to screen renal homogenates from mice in which the gene for the angiotensin II type 1a (AT_1a) receptor has been deleted (versus wild-type mice) to determine which sodium transporters and channels are regulated by the AT_1a receptor at the protein abundance level. In mice maintained on a low NaCl diet (<0.02% NaCl), (1) the abundances of 2 aldosterone-regulated transporters were markedly decreased in knockout versus wild-type mice, namely, the thiazide-sensitive cotransporter and the α-subunit of the amiloride-sensitive Na⁺ channel (α-ENaC); (2) the abundances of β-ENaC and γ-ENaC were markedly increased; and (3) there were no significant changes in the abundances of the proximal tubule Na+-H⁺ exchanger or the Na⁺-K⁺-2Cl⁻ cotransporter of the thick ascending limb. When the experiment was repeated on higher NaCl diets (0.4% or 6% NaCl), the decrease in α-ENaC abundance persisted, whereas the other changes were abolished. Analysis of serum aldosterone concentration in AT_1a knockout mice and wild-type mice on the low NaCl diet revealed the absence of a decrease with AT_1a gene deletion (11.8±2.3 nmol/L for knockout mice and 5.7±0.8 nmol/L for wild-type mice [significantly increased]). These results reveal that the AT_1a receptor plays an important role in regulation of Na⁺ transporter and channel proteins in the “post-macula densa” region of the renal tubule via a mechanism that is not dependent on altered circulating aldosterone concentrations.