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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1998-5-28
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pubmed:abstractText |
Inward rectification, an important determinant of cell excitability, can result from channel blockade by intracellular cations, including Ca2+. However, mostly on the basis of indirect arguments, Ca2+-mediated rectification of inward rectifier K+ current (IK1) is claimed to play no role in the mammalian heart. The present study investigates Ca2+-mediated IK1 rectification during the mammalian ventricular action potential. Guinea pig ventricular myocytes were patch-clamped in the whole-cell configuration. The action potential waveform was recorded and then applied to reproduce normal excitation under voltage-clamp conditions. Subtraction currents obtained during blockade of K+ currents by either 1 mmol/L Ba2+ (IBa) or K+-free solution (I0K) were used to estimate IK1. Similar time courses were observed for IBa and I0K; both currents were strongly reduced during depolarization (inward rectification). Blockade of L-type Ca2+ current by dihydropyridines (DHPs) increased systolic IBa and I0K by 50.7% and 254.5%, respectively. beta-Adrenergic stimulation, when tested on I0K, had an opposite effect; ie, it reduced this current by 66.5%. Ryanodine, an inhibitor of sarcoplasmic Ca2+ release, increased systolic IBa by 47.7%, with effects similar to those of DHPs. Intracellular Ca2+ buffering (BAPTA-AM) increased systolic IBa by 87.7% and blunted the effect of DHPs. Thus, IK1 may be significantly reduced by physiological Ca2+ transients determined by both Ca2+ influx and release. Although Ca2+-induced effects may represent only a small fraction of total IK1 rectification, they are large enough to affect excitability and repolarization. They may also contribute to facilitation of early afterdepolarizations by conditions increasing Ca2+ influx.
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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/1,2-bis(2-aminophenoxy)ethane...,
http://linkedlifedata.com/resource/pubmed/chemical/Barium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Dihydropyridines,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Magnesium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0009-7330
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
18
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pubmed:volume |
82
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
947-56
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:9598592-Action Potentials,
pubmed-meshheading:9598592-Animals,
pubmed-meshheading:9598592-Barium,
pubmed-meshheading:9598592-Calcium,
pubmed-meshheading:9598592-Calcium Channel Blockers,
pubmed-meshheading:9598592-Cells, Cultured,
pubmed-meshheading:9598592-Dihydropyridines,
pubmed-meshheading:9598592-Egtazic Acid,
pubmed-meshheading:9598592-Electric Conductivity,
pubmed-meshheading:9598592-Guinea Pigs,
pubmed-meshheading:9598592-Magnesium,
pubmed-meshheading:9598592-Membrane Potentials,
pubmed-meshheading:9598592-Potassium,
pubmed-meshheading:9598592-Receptors, Adrenergic, beta,
pubmed-meshheading:9598592-Sarcoplasmic Reticulum,
pubmed-meshheading:9598592-Ventricular Function
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pubmed:year |
1998
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pubmed:articleTitle |
Dynamic Ca2+-induced inward rectification of K+ current during the ventricular action potential.
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pubmed:affiliation |
Dipartimento di Fisiologia e Biochimica Generali, Università degli Studi di Milano, Milan, Italy. zanto@imiucca.csi.unimi.it
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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