Linked Life Data

2536449

Source:http://linkedlifedata.com/resource/pubmed/id/2536449

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1B
pubmed:dateCreated
1989-3-9
pubmed:abstractText
Data from in vitro studies show that the mineralocorticoid receptor has an equal affinity for cortisol and aldosterone. This contrasts with the well known selectivity of aldosterone for binding to tissues such as the kidney despite the much higher circulating levels of glucocorticoids. This paper puts forward the hypothesis that the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) is responsible for determining this selectivity. Congenital or acquired deficiency of this enzyme results in a failure of the normal protective mechanism by which cortisol is converted to cortisone or corticosterone to 11-dehydrocorticosterone. As a result the receptor is exposed to cortisol or corticosterone in high concentration which results in sodium retention and potassium loss. In contrast the hippocampal type 1 receptor is associated with much lower 11 beta-OHSD activity and is thus not aldosterone-selective.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-4731
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
213-6
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
The specificity of the human mineralocorticoid receptor: clinical clues to a biological conundrum.
pubmed:affiliation
Department of Medicine, Western General Hospital, Edinburgh, Scotland.
pubmed:publicationType
Journal Article, Review