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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2 Pt 1
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pubmed:dateCreated |
1997-9-24
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pubmed:abstractText |
We report the electrophysiological and functional properties of Ca(2+)-activated Cl- currents [ICl(Ca)] in rat pulmonary artery smooth muscle and the activation of these currents by the metabolic inhibitor cyanide. Caffeine and norepinephrine (NE) evoked both Ca(2+)-activated K+ currents [IK(Ca)] and ICl(Ca) currents in voltage-clamped myocytes (-50 mV). Niflumic acid (10 microM) reduced the caffeine-induced ICl(Ca) by approximately 64% and reversibly reduced NE-induced tension. Exposure of myocytes to cyanide (2-10 mM) induced a slowly developing inward current (-50 mV) in physiological and K(+)-free solutions, which was identified as ICl(Ca) on the basis of ion selectivity and Ca2+ dependence. Cyanide elevated cytosolic Ca2+ concentration, and this elevation was markedly inhibited by preexposure to caffeine and slightly inhibited by nisoldipine. During exposure to caffeine, the Ca(2+)-activated K+ current was also augmented. Cyanide markedly prolonged ICl(Ca) activated by caffeine, increasing the half-decay time from 3.5 (control) to 29 s (cyanide); the half-decay time of the caffeine-induced IK(Ca) was not significantly affected by cyanide. The results indicate that metabolic inhibition increases [Ca2+]i and activates a prolonged, depolarizing Cl- current in pulmonary artery myocytes.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caffeine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Chlorides,
http://linkedlifedata.com/resource/pubmed/chemical/Cyanides,
http://linkedlifedata.com/resource/pubmed/chemical/Niflumic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
273
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
C520-30
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9277349-Animals,
pubmed-meshheading:9277349-Caffeine,
pubmed-meshheading:9277349-Calcium,
pubmed-meshheading:9277349-Chlorides,
pubmed-meshheading:9277349-Cyanides,
pubmed-meshheading:9277349-Cytosol,
pubmed-meshheading:9277349-Electric Conductivity,
pubmed-meshheading:9277349-Female,
pubmed-meshheading:9277349-Male,
pubmed-meshheading:9277349-Muscle, Smooth, Vascular,
pubmed-meshheading:9277349-Niflumic Acid,
pubmed-meshheading:9277349-Norepinephrine,
pubmed-meshheading:9277349-Osmolar Concentration,
pubmed-meshheading:9277349-Pulmonary Artery,
pubmed-meshheading:9277349-Rats,
pubmed-meshheading:9277349-Rats, Sprague-Dawley,
pubmed-meshheading:9277349-Vasoconstrictor Agents
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pubmed:year |
1997
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pubmed:articleTitle |
Ca(2+)-activated Cl- currents are activated by metabolic inhibition in rat pulmonary artery smooth muscle cells.
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pubmed:affiliation |
Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104-6046, USA.
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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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