Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1984-2-27
pubmed:abstractText
Two classes of Ca extrusion mechanisms have been described in animal cells: ATP-driven Ca efflux mediated by a Ca-dependent ATPase, and Na-Ca exchange. The kinetics of the Na-Ca exchange system are modified by ATP. The increase in the carrier's affinity for intracellular Ca appears to be the most important action of ATP. This change in affinity probably involves a phosphorylation step. The ATP-driven Ca efflux and the Na-Ca exchange systems are both present in plasma membranes of squid axons and mammalian cardiac muscle fibers. In these cells, the maximum transport rate through the Na-Ca exchanger is about one order of magnitude greater than the maximum rate mediated by the ATP-driven Ca pump. In barnacle muscle, too, at physiological [Ca2+]in, at most only a small fraction of the Ca efflux is mediated by an ATP-driven Ca pump. Thus, [Ca2+]in appears to be controlled primarily by the Na-Ca exchange system in these cells. Available evidence indicates that the stoichiometry of the exchange system in these cells may be close to 3 Na+:1 Ca2+, so that the electrochemical gradients for the two ions are close to equilibrium. In cardiac muscle, changes in the Na gradient are followed by appropriate changes in the Ca gradient, so that this equilibrium is maintained, as would be predicted for tight chemiosmotic coupling.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0094-7733
pubmed:author
pubmed:issnType
Print
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
129-47
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
The energetics and kinetics of sodium-calcium exchange in barnacle muscles, squid axons, and mammalian heart: the role of ATP.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't