| Aldosterone and mineralocorticoid receptors: orphan questions. | |
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MedLine Citation:
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PMID: 10760067 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Classically, mineralocorticoid receptors (MR) are activated by aldosterone to promote unidirectional transepithelial sodium transport. Activation of MR in nonepithelial tissues has been shown to elevate blood pressure (central nervous system; CNS) and to cause hypertrophy and fibrosis (heart). For both epithelial and nonepithelial tissues, there remain a variety of questions regarding MR which are not only unanswered but also essentially not addressed. Seven such questions include: (1) how the physiologic glucocorticoids (cortisol and corticosterone) can mimic aldosterone action in epithelial MR, but act as antagonists in the heart and AV3V region; (2) how salt facilitates the nonepithelial, pathophysiologic effects of aldosterone; (3) how aldosterone activates unprotected AV3V MR in the face of orders of magnitude higher circulating glucocorticoid concentrations; (4) how unprotected nonepithelial MR act as "always occupied" receptors in guinea pigs and other species; (5) how, when 11beta hydroxysteroid dehydrogenase type 2 is active, epithelial MR occupied by physiologic glucocorticoids appear transcriptionally inactive; (6) how aldosterone activates epithelial MR in the face of approximately 103-fold higher glucocorticoid levels, plasma binding and 11beta hydroxysteroid dehydrogenase type 2 activity notwithstanding; and (7) how aldosterone produces changes in urinary [K+] before [Na+]. |
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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: Kidney international Volume: 57 ISSN: 0085-2538 ISO Abbreviation: Kidney Int. Publication Date: 2000 Apr |
Date Detail:
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Created Date: 2000-05-09 Completed Date: 2000-05-09 Revised Date: 2005-11-16 |
Medline Journal Info:
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Nlm Unique ID: 0323470 Medline TA: Kidney Int Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1358-63 Citation Subset: IM |
Affiliation:
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Baker Medical Research Institute, Melbourne, Australia. sue.smith@baker.edu.au |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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11-beta-Hydroxysteroid Dehydrogenases Aldosterone / physiology Animals Corticosterone / physiology Glucocorticoids / metabolism Hydrocortisone / physiology Hydroxysteroid Dehydrogenases / metabolism Receptors, Aldosterone / physiology* Receptors, Mineralocorticoid / physiology* Sodium Chloride / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Glucocorticoids; 0/Receptors, Aldosterone; 0/Receptors, Mineralocorticoid; 50-22-6/Corticosterone; 50-23-7/Hydrocortisone; 52-39-1/Aldosterone; 7647-14-5/Sodium Chloride; EC 1.1.-/Hydroxysteroid Dehydrogenases; EC 1.1.1.146/11-beta-Hydroxysteroid Dehydrogenases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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