Linked Life Data

16189294

Source:http://linkedlifedata.com/resource/pubmed/id/16189294

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-2-7
pubmed:abstractText
Nephrotic syndrome is often accompanied by sodium retention and generalized edema. We hypothesize that dysregulation of the epithelial sodium channel (ENaC) and/or of sodium (co)transporters may be responsible for the increased sodium retention associated with HgCl(2)-induced nephropathy. In addition, we examined the hypothesis that the expression of type 2 11beta-hydroxysteroid dehydrogenase (11betaHSD2) is reduced, contributing to the enhanced mineralocorticoid activity. Membranous nephropathy was induced in Brown Norway rats by repeated injections of HgCl(2) (1 mg/kg sc), whereas the control group received only vehicle. After 13 days of treatment, the abundance of ENaC subunits, sodium (co)transporters, and 11betaHSD2 in the kidney was examined by immunoblotting and immunohistochemistry. HgCl(2) treatment induced marked proteinuria, hypoalbuminemia, decreased urinary sodium excretion, and ascites. The protein abundance of alpha-ENaC was increased in the cortex/outer stripe of outer medulla (OSOM) and inner stripe of the outer medulla (ISOM). The protein abundances of beta-ENaC and gamma-ENaC were decreased in the cortex/OSOM while increased in the ISOM. Immunoperoxidase microscopy demonstrated increased targeting of ENaC subunits to the apical plasma membrane in the distal convoluted tubule, connecting tubule, and cortical and medullary collecting duct segments. Moreover, 11betaHSD2 abundance was decreased in cortex/OSOM and ISOM. The protein abundances of type 3 Na/H exchanger (NHE3), Na-K-2Cl cotransporter (NKCC2), and thiazide-sensitive Na-Cl cotransporter (NCC) were decreased. Moreover, the abundance of the alpha-1 subunit of the Na-K-ATPase was decreased in the cortex/OSOM and ISOM but remained unchanged in the inner medulla. These results suggest that increased apical targeting of ENaC subunits combined with diminished abundance of 11betaHSD2 may contribute to sodium retention associated with HgCl(2)-induced nephrotic syndrome. The decreased abundance of NHE3, NKCC2, NCC, and Na-K-ATPase may play a compensatory role in promoting sodium excretion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F674-87
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:16189294-11-beta-Hydroxysteroid Dehydrogenase Type 2, pubmed-meshheading:16189294-Animals, pubmed-meshheading:16189294-Disease Models, Animal, pubmed-meshheading:16189294-Epithelial Sodium Channel, pubmed-meshheading:16189294-Gene Expression Regulation, pubmed-meshheading:16189294-Gene Expression Regulation, Enzymologic, pubmed-meshheading:16189294-Kidney, pubmed-meshheading:16189294-Kidney Cortex, pubmed-meshheading:16189294-Kidney Medulla, pubmed-meshheading:16189294-Male, pubmed-meshheading:16189294-Mercuric Chloride, pubmed-meshheading:16189294-Mineralocorticoids, pubmed-meshheading:16189294-Nephrotic Syndrome, pubmed-meshheading:16189294-Protein Subunits, pubmed-meshheading:16189294-Rats, pubmed-meshheading:16189294-Rats, Inbred BN, pubmed-meshheading:16189294-Reference Values, pubmed-meshheading:16189294-Sodium, pubmed-meshheading:16189294-Sodium Channels
pubmed:year
2006
pubmed:articleTitle
Increased apical targeting of renal ENaC subunits and decreased expression of 11betaHSD2 in HgCl2-induced nephrotic syndrome in rats.
pubmed:affiliation
The Water and Salt Research Center, Bldg. 233/234, University of Aarhus, DK-8000 Aarhus C, Denmark.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Intramural