This minireview examines both the basic science and clinical observations over the past 20
years to show how and why overstimulation of the amiloride-sensitive epithelial Na+
channel (ENaC) expressed by epithelial principal cells of the renal collecting duct may be
responsible for a large portion of hypertension in modern society. This idea is based on the
finding that, in Liddle syndrome, a mutation of the β-and/or γ-subunits of ENaC produces an
activated ion channel, in turn resulting in severe hypertension that is resistant to most forms …