Source:http://linkedlifedata.com/resource/pubmed/id/11205054
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2001-2-6
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pubmed:abstractText |
Endothelins have been reported to exert a wide range of electrophysiological effects in mammalian cardiac cells. These results are controversial and human data are not available. Our aim was to study the effects of endothelin-1 (ET-1, 8 nmol/l) on the L-type calcium current (ICa-L) and various potassium currents (rapid component of the delayed rectifier, IKr; transient outward current, Ito; and the inward rectifier K current, IK1) in isolated human ventricular cardiomyocytes. Cells were obtained from undiseased donor hearts using collagenase digestion via the segment perfusion technique. The whole-cell configuration of the patch-clamp technique was applied to measure ionic currents at 37 degrees C. ET-1 significantly decreased peak ICa-L from 10.2+/-0.6 to 6.8+/-0.8 pA/pF at +5 mV (66.7% of control, P<0.05, n=5). This reduction of peak current was accompanied by a lengthening of inactivation. The voltage dependence of steady-state activation and inactivation was not altered by ET- 1. IKr, measured as tail current amplitudes at 40 mV, decreased from 0.31+/-0.02 to 0.06+/-0.02 pA/pF (20.3% of control, P<0.05, n=4) after exposure to ET-1. ET-1 failed to change the peak amplitude of Ito, measured at +50 mV (9.3+/-4.6 and 9.0+/-4.4 pA/pF before and after ET-1, respectively), or steady-state IK1 amplitude, measured at the end of a 400-ms hyperpolarization to -100 mV (3.6+/-1.4 and 3.7+/-1.4 pA/pF, n=4). The present results indicate that in undiseased human ventricular myocytes ET-1 inhibits both ICa-L and IKr; however, the degree of suppression of the two currents is different.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0031-6768
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
441
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
144-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11205054-Action Potentials,
pubmed-meshheading:11205054-Adrenergic beta-Agonists,
pubmed-meshheading:11205054-Calcium Channels, L-Type,
pubmed-meshheading:11205054-Electric Conductivity,
pubmed-meshheading:11205054-Endothelin-1,
pubmed-meshheading:11205054-Heart,
pubmed-meshheading:11205054-Humans,
pubmed-meshheading:11205054-Isoproterenol,
pubmed-meshheading:11205054-Myocardium,
pubmed-meshheading:11205054-Patch-Clamp Techniques,
pubmed-meshheading:11205054-Potassium Channels
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pubmed:year |
2000
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pubmed:articleTitle |
Effects of endothelin-1 on calcium and potassium currents in undiseased human ventricular myocytes.
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pubmed:affiliation |
Department of Physiology, University Medical School of Debrecen, Hungary.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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