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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
1990-12-19
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pubmed:abstractText |
1. Stimulation-dependent modulation of Ca currents was examined in guinea-pig ventricular myocytes at room temperature. Whole-cell recordings of Ca currents were made under conditions which minimized ionic fluxes through other channels. 2. Stimulation from rest at a rate of 2 Hz resulted in a decrease of the low threshold Ca current within one pulse and facilitation of the high threshold Ca current within five pulses. Facilitation was associated with a reduction in the rate of inactivation. 3. Pulse durations as short as 10 ms facilitated the high threshold Ca current in subsequent pulses. Facilitation produced by a single pulse decayed with a half-time of several seconds. 4. Substitution of Ba2+ or Sr2+ for external Ca2+ reduced the rate of inactivation of the high threshold Ca current and abolished facilitation of the current. 5. Facilitation persisted with 40 microM-Ruthenium Red added to the internal solution or 0.2-2 microM-ryanodine added to the bath solution to reduce Ca2+ release from the sarcoplasmic reticulum. 6. Facilitation was modulated by isoprenaline. Low concentrations of isoprenaline (5-10 nM) increased the amount of facilitation. Isoprenaline (1 microM) increased the Ca current approximately 3-fold, however, facilitation was nearly abolished. 7. Caffeine (0.5 and 1 mM) affected the Ca current and facilitation in a manner similar to 1 microM-isoprenaline. It increased the Ca currents approximately 2.5-fold and facilitation was not observed. 8. We conclude that stimulation-dependent facilitation of the high threshold Ca current is mediated by calcium and hypothesize that calcium affects a site near the Ca channel that modifies the rate of inactivation. The common actions of caffeine and high concentrations of isoprenaline suggest that calcium modulates a phosphorylation step.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2411846,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2411919,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2424010,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2425366,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2427730,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2436824,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2443659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2456166,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2459373,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2459777,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2476559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2539269,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2845814,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2855436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2855642,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-2998207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-3127576,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-3608108,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-3722165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-533865,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-6320002,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-6331434,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/2172526-6770893
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-3751
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
428
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
653-71
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2172526-Animals,
pubmed-meshheading:2172526-Caffeine,
pubmed-meshheading:2172526-Calcium Channels,
pubmed-meshheading:2172526-Cell Separation,
pubmed-meshheading:2172526-Electrophysiology,
pubmed-meshheading:2172526-Guinea Pigs,
pubmed-meshheading:2172526-Heart Ventricles,
pubmed-meshheading:2172526-Isoproterenol,
pubmed-meshheading:2172526-Ryanodine,
pubmed-meshheading:2172526-Sarcoplasmic Reticulum,
pubmed-meshheading:2172526-Ventricular Function
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pubmed:year |
1990
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pubmed:articleTitle |
Stimulation-dependent facilitation of the high threshold calcium current in guinea-pig ventricular myocytes.
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pubmed:affiliation |
Department of Physiology, Oregon Health Sciences University, Portland 97201.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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