Sodium reabsorption via ENaC in the aldosterone-sensitive distal nephron (ASDN) is one of the major factors that regulate natriuresis and water-electrolyte balance in the organism. In pathological conditions, increased ENaC activity is associated with improper sodium handling, edema, excessive fluid retention, and hypertension. For instance, hypertension is typical for patients with Liddle's syndrome caused by gain-of-function mutations in ENaC (Hansson et al., 1995). We and others have shown that in Dahl SS rats abnormal activation of ENaC on a high salt diet contributes to the development of hypertension (Kakizoe et al., 2009; Pavlov et al., 2013; Pavlov and Staruschenko, 2016).