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The epithelial Na+ channel: progressing from Liddle's syndrome to essential hypertension.

The amiloride-sensitive epithelial sodium channel (ENaC) is expressed in the distal part of the renal tubule where it constitutes the rate-limiting step of Naþ reabsorption, under the control of aldosterone [1]. Activating mutations of the [2] and a [3] subunits of ENaC lead to increased Naþ and water reabsorption and are at the origin of the rare form of autosomal dominant hypertension (HTN) described by Liddle in 1963 [4]. The classical description of Liddle’s syndrome includes early severe HTN with hypokalemia, metabolic alkalosis and suppressed plasma renin activity (PRA) and aldosterone. These abnormalities are corrected by low Naþ diet associated with amiloride, a specific blocker of ENaC, but not by spironolactone [4].