rdf:type |
|
lifeskim:mentions |
umls-concept:C0030685,
umls-concept:C0391871,
umls-concept:C0521116,
umls-concept:C0596235,
umls-concept:C0597484,
umls-concept:C0678640,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1444748,
umls-concept:C1879547,
umls-concept:C1963578,
umls-concept:C2339371,
umls-concept:C2348693
|
pubmed:issue |
7
|
pubmed:dateCreated |
2008-3-13
|
pubmed:abstractText |
The possible contribution of Na(+)-Ca(2+) exchange to the triggering of Ca(2+) release from the sarcoplasmic reticulum in ventricular cells remains unresolved. To gain insight into this issue, we measured the "trigger flux" of Ca(2+) crossing the cell membrane in rabbit ventricular myocytes with Ca(2+) release disabled pharmacologically. Under conditions that promote Ca(2+) entry via Na(+)-Ca(2+) exchange, internal [Na(+)] (10 mM), and positive membrane potential, the Ca(2+) trigger flux (measured using a fluorescent Ca(2+) indicator) was much greater than the Ca(2+) flux through the L-type Ca(2+) channel, indicating a significant contribution from Na(+)-Ca(2+) exchange to the trigger flux. The difference between total trigger flux and flux through L-type Ca(2+) channels was assessed by whole-cell patch-clamp recordings of Ca(2+) current and complementary experiments in which internal [Na(+)] was reduced. However, Ca(2+) entry via Na(+)-Ca(2+) exchange measured in the absence of L-type Ca(2+) current was considerably smaller than the amount inferred from the trigger flux measurements. From these results, we surmise that openings of L-type Ca(2+) channels increase [Ca(2+)] near Na(+)-Ca(2+) exchanger molecules and activate this protein. These results help to resolve seemingly contradictory results obtained previously and have implications for our understanding of the triggering of Ca(2+) release in heart cells under various conditions.
|
pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-10620297,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-11222287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-1311127,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-1484286,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-15975978,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-1659502,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-2158147,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-2549177,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-7754384,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-8145151,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-8235594,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-8782114,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-9400385,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18223001-9649393
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
1542-0086
|
pubmed:author |
|
pubmed:issnType |
Electronic
|
pubmed:day |
1
|
pubmed:volume |
94
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
L54-6
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:18223001-Animals,
pubmed-meshheading:18223001-Calcium,
pubmed-meshheading:18223001-Calcium Channels, L-Type,
pubmed-meshheading:18223001-Calcium Signaling,
pubmed-meshheading:18223001-Cells, Cultured,
pubmed-meshheading:18223001-Heart Ventricles,
pubmed-meshheading:18223001-Ion Channel Gating,
pubmed-meshheading:18223001-Myocytes, Cardiac,
pubmed-meshheading:18223001-Rabbits,
pubmed-meshheading:18223001-Sarcoplasmic Reticulum,
pubmed-meshheading:18223001-Sodium,
pubmed-meshheading:18223001-Sodium-Calcium Exchanger,
pubmed-meshheading:18223001-Ventricular Function
|
pubmed:year |
2008
|
pubmed:articleTitle |
Allosteric activation of Na+-Ca2+ exchange by L-type Ca2+ current augments the trigger flux for SR Ca2+ release in ventricular myocytes.
|
pubmed:publicationType |
Letter,
Research Support, N.I.H., Extramural
|