Regulation of blood pressure and renal function by NCC and ENaC: lessons from genetically engineered mice

Curr Opin Pharmacol. 2015 Apr:21:60-72. doi: 10.1016/j.coph.2014.12.012. Epub 2015 Jan 20.


The activity of the thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) and of the amiloride-sensitive epithelial Na(+) channel (ENaC) is pivotal for blood pressure regulation. NCC is responsible for Na(+) reabsorption in the distal convoluted tubule (DCT) of the nephron, while ENaC reabsorbs the filtered Na(+) in the late DCT and in the cortical collecting ducts (CCD) providing the final renal adjustment to Na(+) balance. Here, we aim to highlight the recent advances made using transgenic mouse models towards the understanding of the regulation of NCC and ENaC function relevant to the control of sodium balance and blood pressure. We thus like to pave the way for common mechanisms regulating these two sodium-transporting proteins and their potential implication in structural remodeling of the nephron segments and Na(+) and Cl(-) reabsorption.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Blood Pressure / physiology*
  • Epithelial Sodium Channels / physiology*
  • Humans
  • Insulin / physiology
  • Kidney / physiology*
  • Mice, Transgenic
  • Minor Histocompatibility Antigens
  • Protein Serine-Threonine Kinases / physiology
  • Renin-Angiotensin System / physiology
  • Solute Carrier Family 12, Member 3 / physiology
  • Vasopressins / physiology
  • WNK Lysine-Deficient Protein Kinase 1


  • Epithelial Sodium Channels
  • Insulin
  • Minor Histocompatibility Antigens
  • Slc12a3 protein, mouse
  • Solute Carrier Family 12, Member 3
  • Vasopressins
  • Protein Serine-Threonine Kinases
  • WNK Lysine-Deficient Protein Kinase 1
  • Wnk1 protein, mouse