Linked Life Data

20719974

Source:http://linkedlifedata.com/resource/pubmed/id/20719974

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-11-4
pubmed:abstractText
Rh B glycoprotein (Rhbg) is a member of the Rh glycoprotein family of ammonia transporters. In the current study, we examine Rhbg's role in basal and acidosis-stimulated acid-base homeostasis. Metabolic acidosis induced by HCl administration increased Rhbg expression in both the cortex and outer medulla. To test the functional significance of increased Rhbg expression, we used a Cre-loxP approach to generate mice with intercalated cell-specific Rhbg knockout (IC-Rhbg-KO). On normal diet, intercalated cell-specific Rhbg deletion did not alter urine ammonia excretion, pH, or titratable acid excretion significantly, but it did decrease glutamine synthetase expression in the outer medulla significantly. After metabolic acidosis was induced, urinary ammonia excretion was significantly less in IC-Rhbg-KO than in control (C) mice on days 2-4 of acid loading, but not on day 5. Urine pH and titratable acid excretion and dietary acid intake did not differ significantly between acid-loaded IC-Rhcg-KO and C mice. In IC-Rhbg-KO mice, acid loading increased connecting segment (CNT) cell and outer medullary collecting duct principal cell Rhbg expression. In both C and IC-Rhbg-KO mice, acid loading decreased glutamine synthetase in both the cortex and outer medulla; the decrease on day 3 was similar in IC-Rhbg-KO and C mice, but on day 5 it was significantly greater in IC-Rhbg-KO than in C mice. We conclude 1) intercalated cell Rhbg contributes to acidosis-stimulated renal ammonia excretion, 2) Rhbg in CNT and principal cells may contribute to renal ammonia excretion, and 3) decreased glutamine synthetase expression may enable normal rates of ammonia excretion under both basal conditions and on day 5 of acid loading in IC-Rhbg-KO mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1522-1466
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
299
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F1065-77
pubmed:dateRevised
2011-11-1
pubmed:meshHeading
pubmed-meshheading:20719974-Acidosis, pubmed-meshheading:20719974-Acids, pubmed-meshheading:20719974-Alleles, pubmed-meshheading:20719974-Ammonia, pubmed-meshheading:20719974-Animals, pubmed-meshheading:20719974-Bicarbonates, pubmed-meshheading:20719974-Blotting, Western, pubmed-meshheading:20719974-Diet, pubmed-meshheading:20719974-Electrolytes, pubmed-meshheading:20719974-Gene Deletion, pubmed-meshheading:20719974-Gene Expression Regulation, Enzymologic, pubmed-meshheading:20719974-Glutamate-Ammonia Ligase, pubmed-meshheading:20719974-Glycoproteins, pubmed-meshheading:20719974-Immunohistochemistry, pubmed-meshheading:20719974-Kidney, pubmed-meshheading:20719974-Membrane Transport Proteins, pubmed-meshheading:20719974-Mice, pubmed-meshheading:20719974-Mice, Inbred C57BL, pubmed-meshheading:20719974-Mice, Knockout, pubmed-meshheading:20719974-Mice, Transgenic, pubmed-meshheading:20719974-Potassium
pubmed:year
2010
pubmed:articleTitle
Role of the Rhesus glycoprotein, Rh B glycoprotein, in renal ammonia excretion.
pubmed:affiliation
Div. of Nephrology, Hypertension, and Transplantation, P.O. Box 100224, Univ. of Florida College of Medicine, Gainesville, FL 32610-0224, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural