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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4 Pt 2
|
| pubmed:dateCreated |
1998-11-19
|
| pubmed:abstractText |
To determine whether there are abnormalities in myocyte excitation-contraction coupling and intracellular Ca2+ concentration ([Ca2+]i) homeostasis in pacing-induced heart failure (PF), we measured L-type Ca2+ current (ICa,L) and Na+/Ca2+ exchanger current (INa/Ca) with voltage clamp and measured intracellular Na+ concentration ([Na+]i) and [Ca2+]i with the use of sodium-binding benzofuran isophthalate (SBFI) and fluo 3 in ventricular myocytes isolated from control and paced rabbits. The peak systolic and diastolic levels and the amplitude of electrically stimulated [Ca2+]i transients (0.25 Hz, extracellular Ca2+ concentration = 1.08 mM) were significantly less in PF myocytes. Also, there was prolongation of the times to peak and decline of [Ca2+]i transients. ICa,L density was markedly decreased in PF myocytes. INa/Ca at -40 mV elicited by rapid exposure to 0 Na+ solution with a rapid solution switcher was significantly reduced in PF myocytes, suggesting that the function of the Na+/Ca2+ exchanger is impaired in these myocytes. In PF myocytes the decline of the [Ca2+]i transient when the Na+/Ca2+ exchanger was abruptly disabled was markedly prolonged compared with the decline in control myocytes, consistent with depressed sarcoplasmic reticulum (SR) Ca2+-ATPase function. RNase protection assay showed decreased levels of Na+/Ca2+ exchanger and SR Ca2+-ATPase mRNA in PF hearts, consistent with the function studies. We conclude that the functions of L-type Ca2+ channels, Na+/Ca2+ exchanger, and SR Ca2+-ATPase are impaired in myocytes from rabbit hearts with failure induced by rapid pacing. These abnormalities result in reduced [Ca2+]i transients and systolic and diastolic dysfunction and appear to account for the abnormal ventricular function observed.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Transporting ATPases,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Calcium Exchanger
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0002-9513
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
275
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
H1441-8
|
| pubmed:dateRevised |
2010-11-18
|
| pubmed:meshHeading |
pubmed-meshheading:9746495-Animals,
pubmed-meshheading:9746495-Blood Pressure,
pubmed-meshheading:9746495-Body Weight,
pubmed-meshheading:9746495-Calcium,
pubmed-meshheading:9746495-Calcium Channels,
pubmed-meshheading:9746495-Calcium Channels, L-Type,
pubmed-meshheading:9746495-Calcium-Transporting ATPases,
pubmed-meshheading:9746495-Cells, Cultured,
pubmed-meshheading:9746495-Heart,
pubmed-meshheading:9746495-Heart Failure,
pubmed-meshheading:9746495-Homeostasis,
pubmed-meshheading:9746495-Kinetics,
pubmed-meshheading:9746495-Myocardium,
pubmed-meshheading:9746495-Organ Size,
pubmed-meshheading:9746495-Pacemaker, Artificial,
pubmed-meshheading:9746495-Patch-Clamp Techniques,
pubmed-meshheading:9746495-Rabbits,
pubmed-meshheading:9746495-Reference Values,
pubmed-meshheading:9746495-Sarcoplasmic Reticulum,
pubmed-meshheading:9746495-Sodium,
pubmed-meshheading:9746495-Sodium-Calcium Exchanger
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Abnormal myocyte Ca2+ homeostasis in rabbits with pacing-induced heart failure.
|
| pubmed:affiliation |
Division of Cardiology, University of Utah Health Sciences Center, Salt Lake City, Utah 84132, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|