ENaC-mediated sodium reabsorption in the collecting duct (CD) is a critical determinant of urinary sodium excretion. Existing evidence suggest direct stimulatory actions of Angiotensin II (Ang II) on ENaC in the CD, independently of the aldosterone- mineralocorticoid receptor (MR) signaling. Deletion of the major renal AT(1) receptor isoform, AT(1a)R, decreases blood pressure and reduces ENaC abundance despite elevated aldosterone levels. The mechanism of this insufficient compensation is not known. Here, we used patch clamp electrophysiology in freshly isolated split-opened CDs to investigate how AT(1a)R dysfunction compromises functional ENaC activity and its regulation by dietary salt intake. Ang II had no effect on ENaC activity in CDs from AT(1a)R −/− mice suggesting no complementary contribution of AT(2) receptors. We next found that AT(1a)R deficient mice had lower ENaC activity when fed with low (