| Implication of ENaC in salt-sensitive hypertension. | |
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MedLine Citation:
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PMID: 10419016 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Arterial blood pressure is critically dependent on sodium balance. The kidney is the key player in maintaining sodium homeostasis. Aldosterone-dependent epithelial sodium transport in the distal nephron is mediated by the highly selective, amiloride-sensitive epithelial sodium channel (ENaC). Direct evidence that dysfunction of ENaC participates in blood pressure regulation has come from the molecular analysis of two human genetic diseases, Liddle's syndrome and pseudohypoaldosteronism type 1 (PHA-1). Both, increased sodium reabsorption despite low aldosterone levels in Liddle's patients and decreased sodium reabsorption despite high aldosterone levels in PHA-1 patients, demonstrated that ENaC is an effector for aldosterone action. Gene-targeting and classical transgenic technology enable the generation of mouse models for these diseases and the analysis of the involvement of the epithelial sodium channel (ENaC) in the progress of these diseases. A first mouse model using alphaENaC transgenic knockout mice [alphaENaC(-/-)Tg] mimicked several clinical features of PHA-1, like salt-wasting, metabolic acidosis, high aldosterone levels, growth retardation and increased early mortality. Such mouse models will be necessary in testing the involvement of genetic and/or environmental factors like salt-intake in hypertension. |
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Authors:
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E Hummler |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: The Journal of steroid biochemistry and molecular biology Volume: 69 ISSN: 0960-0760 ISO Abbreviation: J. Steroid Biochem. Mol. Biol. Publication Date: 1999 Apr-Jun |
Date Detail:
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Created Date: 1999-08-02 Completed Date: 1999-08-02 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9015483 Medline TA: J Steroid Biochem Mol Biol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 385-90 Citation Subset: IM |
Affiliation:
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Institut de Pharmacologie et de Toxicologie, Université de Lausanne, Switzerland. ehummler@pop-server.unil.ch |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aldosterone
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physiology Animals Biological Transport Disease Models, Animal Epithelial Sodium Channel Humans Hypertension / physiopathology* Pseudohypoaldosteronism / physiopathology Renin-Angiotensin System Sodium Channels / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Epithelial Sodium Channel; 0/Sodium Channels; 52-39-1/Aldosterone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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