Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-2-8
pubmed:abstractText
We examined the role of glucocorticoids in the activity of the renal brush border Na-H antiporter under baseline conditions (5% CO2 gassing) and during respiratory acidosis (10% CO2 gassing) in cultured monolayers of a proximal tubule suspension (primary cultures of the proximal tubule). Primary cultures of the proximal tubule showed an adaptive increase in renal brush border Na-H antiporter activity in response to respiratory acidosis in presence but not in the absence of physiologic concentrations of hydrocortisone in the medium. The effect of hydrocortisone to increase the activity of the renal brush border Na-H antiporter in respiratory acidosis could also be elicited by dexamethasone. Deletion of hydrocortisone from the medium also impaired the baseline activity of the Na-H antiporter. The effect of hydrocortisone to increase the activity of the Na-H antiporter under baseline conditions and during respiratory acidosis was elicited by physiologic concentrations of the hormone and 100-fold increase in concentration did not further increase the activity of the Na-H antiporter. These results demonstrate that the presence of physiologic concentrations of glucocorticoids are necessary for the baseline activity of the renal brush border Na-H antiporter and its adaptive increase in response to respiratory acidosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0167-0115
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
329-36
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Glucocorticoids and the renal Na-H antiporter: role in respiratory acidosis.
pubmed:affiliation
Section of Nephrology, College of Medicine, University of Illinois at Chicago 60612.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.