It is intriguing that expression of α-ENaC but not β- or γ-subunit was elevated in the renal inner medulla but not renal cortex of floxed mice following Ang II infusion, and this elevation was completely blocked by CD PRR deletion.16 These results suggest that PRR-dependent activation of ENaC-mediated Na+ reabsorption in the terminal nephron segment may in part contribute to Ang II–induced hypertension. Here, AGT is linked to Hypertension.