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rdf:type |
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lifeskim:mentions |
umls-concept:C0030685,
umls-concept:C0127400,
umls-concept:C0178719,
umls-concept:C0205042,
umls-concept:C0253216,
umls-concept:C0288250,
umls-concept:C0391871,
umls-concept:C0596235,
umls-concept:C0680255,
umls-concept:C1135183,
umls-concept:C1135918,
umls-concept:C1283071,
umls-concept:C1879547,
umls-concept:C1963578
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pubmed:issue |
4
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pubmed:dateCreated |
2001-2-22
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pubmed:abstractText |
1. Effects of NS-1619, an opener of large conductance Ca2+-activated K+ (BK) channel, on intracellular Ca2+ concentration ([Ca2+]i) and membrane potential were examined in single myocytes freshly isolated from porcine coronary artery. 2. Under current clamp mode, the application of 1-30 microM NS-1619 hyperpolarized the membrane in concentration-dependent manner. The NS-1619-induced hyperpolarization was abolished by the presence of 100 nM iberiotoxin. 3. Application of 1-10 microM NS-1619 hyperpolarized the membrane by approximately 6 mV or less but did not change significantly the [Ca2+]i. When membrane hyperpolarization of 12 mV or so was caused by 30 microM NS-1619, [Ca2+]i was unexpectedly increased by approximately 200 nM. This increase in [Ca2+]i and the concomitant outward current activation were also observed under voltage-clamp at holding potential of -40 mV. 4. The increase in [Ca2+]i by 30 microM NS-1619 occurred mainly in peripheral regions than in the centre of the myocytes. The removal of extracellular Ca2+ affected neither the membrane hyperpolarization nor the increase in [Ca2+]i. 5. In the presence of 10 mM caffeine and 10 microM ryanodine, the increase in [Ca2+]i by 30 microM NS-1619 was not observed and the membrane hyperpolarization was reduced to approximately 67% of the control. 6. These results indicate that the opening of BK channels by NS-1619 at 30 microM, which is the most frequently used concentration of this agent, is partly due to Ca2+ release from caffeine/ryanodine-sensitive intracellular storage sites but is mainly due to the direct activation of the channels.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-10446750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-10490897,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-2482352,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7517630,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7534190,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7535111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7570021,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7589189,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7647022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7685635,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7733230,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7792935,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7858852,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-7965736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8064354,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8137869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8371147,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8564233,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8760027,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8772460,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8825352,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8889205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-8935724,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9151934,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9228665,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9399993,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9660887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9674696,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9694955,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9758866,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9920798,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9925820,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11181423-9925821
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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 |
Feb
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pubmed:issn |
0007-1188
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
132
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
828-34
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
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pubmed:year |
2001
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pubmed:articleTitle |
BK channel activation by NS-1619 is partially mediated by intracellular Ca2+ release in smooth muscle cells of porcine coronary artery.
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pubmed:affiliation |
Department of Molecular and Cellular Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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