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The epithelial sodium channel: from molecule to disease.
Journal article

The epithelial sodium channel: from molecule to disease.

  • Schild L Department of Pharmacology and Toxicology, University of Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland. Laurent.Schild@ipharm.unil.ch
  • 2004-05-18
Published in:
  • Reviews of physiology, biochemistry and pharmacology. - 2004
Aldosterone
Amino Acid Motifs
Animals
Biological Transport
Epithelial Sodium Channels
Humans
Kidney
Mutation
Proline
Salts
Sodium
Sodium Channels
English Genetic analysis has demonstrated that Na absorption in the aldosterone-sensitive distal nephron (ASDN) critically determines extracellular blood volume and blood pressure variations. The epithelial sodium channel (ENaC) represents the main transport pathway for Na+ absorption in the ASDN, in particular in the connecting tubule (CNT), which shows the highest capacity for ENaC-mediated Na+ absorption. Gain-of-function mutations of ENaC causing hypertension target an intracellular proline-rich sequence involved in the control of ENaC activity at the cell surface. In animal models, these ENaC mutations exacerbate Na+ transport in response to aldosterone, an effect that likely plays an important role in the development of volume expansion and hypertension. Recent studies of the functional consequences of mutations in genes controlling Na+ absorption in the ASDN provide a new understanding of the molecular and cellular mechanisms underlying the pathogenesis of salt-sensitive hypertension.
Language
  • English
Open access status
closed
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Persistent URL
https://sonar.ch/global/documents/98735
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