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(Hypertension. 2008;52:595.)
© 2008 American Heart Association, Inc.

Brief Reviews

Epithelial Sodium Channel

Mendelian Versus Essential Hypertension

From the Department of Pharmacology and Toxicology, University of Lausanne, Switzerland.

Correspondence to Bernard C. Rossier, Department of Pharmacology and Toxicology, University of Lausanne, Rue du Bugnon 27, CH-1005, Switzerland. E-mail bernard.rossier@unil.ch

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Despite large changes in water and salt intake, the kidney is able to maintain the extracellular osmolarity and volume within narrow margins.¹ Such fine control requires specific factors or hormones; among them, aldosterone and vasopressin play key roles. In aldosterone-responsive epithelial cells (kidney, colon), the epithelial sodium channel (ENaC) plays a critical role in the control of sodium balance, blood volume, and blood pressure.¹ Tissue-specific expression of ENaC is observed in sodium transporting epithelia (lung, intestine, kidney, and exocrine and sweat glands). In lung, ENaC has a distinct role in controlling the ionic composition of the air liquid interface and thus the rate of mucociliary transport. ENaC subunits are found in the aldosterone-sensitive distal nephron (ASDN; Figure), in the surface epithelia of the colon, and in the duct cells of exocrine glands. In human, imbalance of ENaC activity in aldosterone target cells leads to a large variety of pathologies:² loss of function of ENaC leads to a severe renal salt loosing syndrome, with a hypotensive phenotype (pseudohypoaldosteronism type 1), whereas ENaC gain of function leads to hypertension (Liddle’s syndrome).

View larger version (48K):   Figure. Model of aldosterone action in the principal cell of the ASDN. Aldosterone binds to its cognate mineralocorticoid receptor (MR) and is translocated into the nucleus, where it binds to the promoter of specific genes leading to the repression (ART) or induction (AIT) of mRNA transcripts (ENaC, NaK-ATPase, and Sgk-1). Sgk-1, in turn, regulates the activity of E3 ubiquitin ligase (Nedd4-2), leading to increased ENaC activity at the cell surface.1

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