[14] Similarly, inner medullary collecting duct cells treated with low salt medium had increased α-ENaC expression that was reversed by PRR shRNA.[14] Recent work by Ramkumar et al using the same nephron specific PRR knockout model as in the current study, also demonstrated that under baseline conditions knockout of PRR in the nephron resulted in decreased α-ENaC expression.[28] To our knowledge, however, the current study is the first to show increased renal PRR in the setting of obesity and that this in turn mediates obesity related increases in BP via α-ENaC. Here, ATP6AP2 is linked to obesity due to melanocortin 4 receptor deficiency.