Linked Life Data

9431846

Source:http://linkedlifedata.com/resource/pubmed/id/9431846

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12 Pt 1
pubmed:dateCreated
1998-2-20
pubmed:abstractText
The nature of the cellular abnormality causing hypokalemia, hypotension, and hypovolemia in Bartter's and Gitelman's syndromes is still being debated. In fact, despite the recent descriptions of an array of nonconservative missense or point mutations in some ion transporters and in K+ channel, the lack of detectable defects in some patients suggests that other abnormalities of cell ion homeostasis may be involved in the pathophysiology of these syndromes. The study of the activity of cell ion transporters in patients with these syndromes using red blood cells (RBC) as a cellular model never investigated the role of plasma factor(s) affecting ion transport.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0263-6352
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1407-13
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Inhibition of furosemide-sensitive cation transport and activation of sodium-lithium exchange by endogenous circulating factor(s) in Bartter's and Gitelman's syndromes.
pubmed:affiliation
Institute of Internal Medicine, Division of Nephrology, University of Padova, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't