Linked Life Data

7694338

Source:http://linkedlifedata.com/resource/pubmed/id/7694338

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1993-11-26
pubmed:abstractText
The activities of three mitochondrial oxidative enzymes (citrate synthase, 3-ketoacid-CoA transferase, beta-hydroxyacyl-CoA dehydrogenase) and Na-K-ATPase were microassayed in isolated segments of the rat proximal convoluted tubule (PCT) and medullary thick ascending limb of the loop of Henle (mTAL). The effects of adrenalectomy (ADX) and ADX plus exogenous glucocorticoids were analyzed. The hormonal replacement was daily injections of dexamethasone (10 micrograms/100 g body weight/24 h) for 5 days. ADX lowered the activity of all oxidative enzymes studies in the mTAL, but not in the PCT and led to a decrease in Na-K-ATPase in both nephron segments. Dexamethasone restored the normal level of oxidative enzymes and Na-K-ATPase in the mTAL and of Na-K-ATPase in the PCT. We conclude that the activities of citrate synthase, 3-ketoacid-CoA transferase and beta-hydroxyacyl-CoA dehydrogenase and of Na-K-ATPase are coordinately regulated in the mTAL and that glucocorticoids are essential for the long-term regulation of these enzyme activities in this nephron segment. In contrast, the activities of mitochondrial oxidative enzymes are not influenced by glucocorticoids in the PCT. This study presents the first evidence for a cell-specific regulation by glucocorticoids of oxidative metabolism in the nephron of adult rat kidney.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1011-6524
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
249-56
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:articleTitle
Effect of glucocorticoids on mitochondrial oxidative enzyme and Na-K-ATPase activities in the rat proximal tubule and thick ascending limb of Henle.
pubmed:affiliation
INSERM U319, Université Paris 7, France.
pubmed:publicationType
Journal Article