Linked Life Data

10219107

Source:http://linkedlifedata.com/resource/pubmed/id/10219107

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-6-29
pubmed:abstractText
We used fura-2 microfluorometry to investigate the role of mitochondria in regulating the increase in the cytosolic Ca2+ concentration ([Ca]in) and the mechanism(s) underlying the subsequent Ca2+ efflux from mitochondria in bovine adrenal chromaffin cells. The rate of [Ca]in decay during and following stimulation with 100 mM KCl depolarization was markedly increased when the mitochondrial Na+/Ca2+ exchanger was inhibited by clonazepam or CGP-37157(CGP). In contrast, the addition of gramicidin, which increased the cytosolic Na+ concentration, following KCl depolarization caused a secondary increase in [Ca]in. This secondary increase in [Ca]in was prevented by the addition of clonazepam or CGP, and by the removal of external Na+. The subsequent removal of clonazepam or CGP, or the delayed addition of Na+ caused a slow increase in [Ca]in. A protonophore (FCCP) applied following KCl depolarization also caused a robust, secondary increase in [Ca]in, which was insensitive to blocking by clonazepam or CGP. Neither gramicidin nor FCCP altered the [Ca]in decay when applied following stimulation with histamine or caffeine, which mobilized Ca2+ from intracellular stores. These results suggest that the large [Ca]in increase induced by Ca2+ influx, but not by intracellular Ca2+ release, is buffered by mitochondria, and that the mitochondrial Na+/Ca2+ exchanger makes a major contribution to the subsequent Ca2+ efflux from mitochondria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-521X
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
35-46
pubmed:dateRevised
2007-3-21
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Sequestration of depolarization-induced Ca2+ loads by mitochondria and Ca2+ efflux via mitochondrial Na+/Ca2+ exchanger in bovine adrenal chromaffin cells.
pubmed:affiliation
Department of Physiology, Kagoshima University School of Medicine, Kagoshima, 890-8520, Japan. ciliary@med2.kufm.kagoshima-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't