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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1990-8-13
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pubmed:abstractText |
The L-type calcium current was investigated in normal and hypertrophied rat ventricular myocytes as a possible cause of the action potential lengthening that has been reported during hypertrophy. Regulation of the calcium current (ICa) by a beta-adrenergic agonist (isoproterenol) was also analyzed since beta-agonist-induced positive inotropy is less marked in hypertrophied heart. Left ventricular hypertrophy was induced by stenosis of the abdominal aorta. For recording ICa, the whole-cell patch-clamp technique was used. Potassium currents were suppressed by replacing K+ ions with Cs+ ions in both the extracellular and intracellular media, and sodium current was blocked by 50 microM tetrodotoxin. The Ca2+ current was larger in hypertrophied cells (2.2 +/- 0.6 nA [n= 31]) than in normal cells (1.2 +/- 0.5 nA [n = 33]). However, if one relates ICa amplitude to the cell membrane area, as estimated by membrane capacitance measurement, no significant difference was observed in current density (8.5 +/- 2.5 pA/pF [n = 31] and 8.3 +/- 2.1 pA/pF [n = 33] in hypertrophied and in normal cells, respectively). In both cell types, ICa displayed the same voltage and time dependence. When expressed as a percentage, the maximal increase in ICa amplitude that was obtained with 100 nM isoproterenol was less in hypertrophied cells (+78%) than in normal cells (+120%). The sensitivity of ICa to beta-adrenergic stimulation was not modified: EC50 was 3.8 nM for hypertrophied cells and 4.8 nM for normal cells. Forskolin and cyclic AMP were as effective in both cell types. Stimulation of ICa by beta-adrenergic agonist was decreased in agreement with a reduced number of binding sites of beta-agonists and/or an altered coupling of the G-proteins.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0009-7330
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
67
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
199-208
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1973082-Action Potentials,
pubmed-meshheading:1973082-Adrenergic beta-Agonists,
pubmed-meshheading:1973082-Animals,
pubmed-meshheading:1973082-Calcium,
pubmed-meshheading:1973082-Cardiomegaly,
pubmed-meshheading:1973082-Differential Threshold,
pubmed-meshheading:1973082-Electric Conductivity,
pubmed-meshheading:1973082-Heart,
pubmed-meshheading:1973082-Homeostasis,
pubmed-meshheading:1973082-Isoproterenol,
pubmed-meshheading:1973082-Male,
pubmed-meshheading:1973082-Myocardium,
pubmed-meshheading:1973082-Rats,
pubmed-meshheading:1973082-Rats, Inbred Strains,
pubmed-meshheading:1973082-Reference Values
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pubmed:year |
1990
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pubmed:articleTitle |
Calcium current in single cells isolated from normal and hypertrophied rat heart. Effects of beta-adrenergic stimulation.
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pubmed:affiliation |
Laboratoire de Physiologie Cellulaire Cardiaque, INSERM U-241, Université Paris-Sud, Orsay, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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