| Corticosteroid hypertension. | |
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MedLine Citation:
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PMID: 8564448 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Over the past year, the focus in corticosteroid hypertension has been on the cloning of the enzyme 11 beta-hydroxysteroid dehydrogenase, and the demonstration of a variety of mutations or deletions in the sequence coding for this enzyme in the syndrome of apparent mineralocorticoid excess. This syndrome is the third single-gene cause of human hypertension to be characterized, with glucocorticoid remediable aldosteronism (1992) and Liddle's syndrome (1994). The three conditions are characterized by inappropriate control of aldosterone secretion (glucocorticoid remediable aldosteronism), sodium retention (Liddle's syndrome) or aldosterone action (apparent mineralocorticoid excess), and underline a potential role of an aldosterone: salt imbalance in mineralocorticoid hypertension. No comparable mechanisms of hypertension following glucocorticoid receptor occupancy have been documented to date. |
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Authors:
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J W Funder |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Current opinion in nephrology and hypertension Volume: 4 ISSN: 1062-4821 ISO Abbreviation: Curr. Opin. Nephrol. Hypertens. Publication Date: 1995 Sep |
Date Detail:
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Created Date: 1996-03-01 Completed Date: 1996-03-01 Revised Date: 2005-11-16 |
Medline Journal Info:
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Nlm Unique ID: 9303753 Medline TA: Curr Opin Nephrol Hypertens Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 432-7 Citation Subset: IM |
Affiliation:
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Baker Medical Research Institute, Prahran, Victoria, Australia. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adrenal Cortex Hormones
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genetics,
metabolism* Animals Humans Hypertension / etiology*, metabolism Mutation Receptors, Steroid / genetics, metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Adrenal Cortex Hormones; 0/Receptors, Steroid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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