The epithelial sodium channel in hypertension.

Abstract

Our understanding of Na(+) transport defects has exploded in the past several years, and has provided unique insights into epithelial transport processes, and unusual clinical syndromes resulting from mutations of specific ion transporters. These genetic disorders affect Na(+) balance, with both Na(+) retaining and Na(+) wasting conditions being the consequence. A major focus of these studies has been the epithelial sodium channel (ENaC), which can be directly affected by mutations (eg, Liddle syndrome, autosomal recessive pseudohypoaldosteronism, type I) or by changes in the response to (autosomal recessive pseudohypoaldosteronism, type I), or production of mineralocorticoids (apparent mineralocorticoid excess syndrome, glucocorticoid-remediable aldosteronism). As a result, we now have clearly defined syndromes in which ENaC activity is dysregulated with subsequent development of disorders of systemic blood pressure that can be attributed to a primary renal mechanism.

• Authors: D G Warnock
• Journal: Current hypertension reports (Curr Hypertens Rep) 1999 Apr-May Vol. 1 Issue 2 Pg. 158-63 ISSN: 1522-6417 [Print] United States
• PMID: 10981060 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

• Epithelial Sodium Channels
• Mineralocorticoids
• SCNN1B protein, human
• Sodium Channels

Topics

• Epithelial Sodium Channels
• Humans
• Hypertension (genetics, physiopathology)
• Mineralocorticoids (blood)
• Mutation
• Polymorphism, Genetic (genetics)
• Sodium Channels (genetics, physiology)