Linked Life Data

2382703

Source:http://linkedlifedata.com/resource/pubmed/id/2382703

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 1
pubmed:dateCreated
1990-9-11
pubmed:abstractText
Three different types of mitochondrial poisons (oligomycin, antimycin A, and dinitrophenol) strongly inhibited Na(+)-Ca2+ exchange in aortic myocytes. Exchange activity was assayed as 45Ca2+ uptake that depended on inverting the Na+ gradient and was inhibited by 25 microM dimethylbenzamil. Glucose markedly decreased the inhibition of exchange activity by these three poisons. Glucose also prevented rotenone from inhibiting exchange and depleting cellular ATP. In the absence of glucose, rotenone decreased ATP and exchange activity with half-times of 0.8 and 0.9 min, respectively. Almost eliminating cellular ATP with rotenone maximally inhibited exchange by 80%. Repletion of ATP with glucose substantially restored Na(+)-Ca2+ exchange activity. Ca2+ uptake by organelles, subsequent to entry via exchange for Na+, does not appear to contribute significantly to exchange activity as assayed in intact myocytes. The specific activity of Na(+)-Ca2+ exchange was approximately 30 nmol.min-1.mg protein-1. These findings suggest that ATP modulates exchange activity and that there are approximately 150,000 Na(+)-Ca2+ exchangers per cell, assuming that the turnover number is 1,000 s-1.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
259
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C302-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Energy dependence of sodium-calcium exchange in vascular smooth muscle cells.
pubmed:affiliation
Department of Pharmacology, School of Medicine, University of Alabama, Birmingham 35294.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't