Role of the epithelial sodium channel in salt- sensitive hypertension

The epithelial sodium channel （ENaC） is a heteromeric channel composed of three similar but distinct subunits, α, β and γ. This channel is an end-effector in the rennin-angiotensin-aldosterone system and resides in the apical plasma membrane of the renal cortical collecting ducts, where reabsorption of Na＋ through ENaC is the final renal adjustment step for Na＋ balance. Because of its regulation and function, the ENaC plays a critical role in modulating the homeostasis of Na＋ and thus chronic blood pressure. The development of most forms of hypertension requires an increase in Na＋ and water retention. The role of ENaC in developing high blood pressure is exemplified in the gain-of-function mutations in ENaC that cause Liddle＇s syndrome, a severe but rare form of inheritable hypertension The evidence obtained from studies using animal models and in human patients indicates that improper Na＋ retention by the kidney elevates blood pressure and induces salt-sensitive hypertension.