Source:http://linkedlifedata.com/resource/pubmed/id/12500029
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2002-12-24
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pubmed:abstractText |
The aims of this study were to investigate the effects of a selective ETA (BQ-123), a selective ETB (BQ-788), and a specific mixed ETA/ETB receptor antagonist (bosentan) on the pulmonary vasoconstriction induced by hypoxia in the isolated perfused rat lung, and the role of nitric oxide, adenosine triphosphate-sensitive (KATP), large conductance Ca+-activated (BKCa) and 4-aminopyridine-sensitive voltage-gated K channels (K+) in the relaxant effects of the selective ETA receptor antagonist BQ-123 and a protein kinase C inhibitor, bisindolylmaleimide I. K+ channels were inhibited by glibenclamide, charybdotoxin, and 4-aminopyridine and nitric oxide synthase by L-NG-nitroarginine methyl ester (L-NAME). Hypoxic ventilation produced a significant pressure response (+57%, p < 0.001). BQ-123, bosentan, and bisindolylmaleimide I induced a concentration-dependent decrease of the hypoxic pressure response (p < 0.001), whereas BQ-788 did not exhibit any inhibitory effect against hypoxic pressure response. Glibenclamide, charybdotoxin, and 4-aminopyridine partially opposed the inhibitory effects elicited by BQ-123 (p < 0.05), but L-NAME did not modify these effects. The effects of bisindolylmaleimide I on hypoxic pressure response were unaffected by glibenclamide, charybdotoxin, or 4-aminopyridine. The authors conclude that (a) ETA receptors and protein kinase C are involved in the modulation of hypoxic pulmonary vasoconstriction; and (b) the ETA antagonist BQ-123 opposes hypoxic pulmonary vasoconstriction through KATP, KV, and BKCa channels, differing in this from the protein kinase C inhibitor bisindolylmaleimide I. These results suggest that BQ-123 operates through a mechanism independent of bisindolylmaleimide I-inhibited protein kinase C isoforms.
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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/BQ 788,
http://linkedlifedata.com/resource/pubmed/chemical/Indoles,
http://linkedlifedata.com/resource/pubmed/chemical/Maleimides,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides, Cyclic,
http://linkedlifedata.com/resource/pubmed/chemical/Piperidines,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Endothelin,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/bisindolylmaleimide,
http://linkedlifedata.com/resource/pubmed/chemical/bosentan,
http://linkedlifedata.com/resource/pubmed/chemical/cyclo(Trp-Asp-Pro-Val-Leu)
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0160-2446
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
41
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
117-25
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:12500029-Animals,
pubmed-meshheading:12500029-Anoxia,
pubmed-meshheading:12500029-Drug Interactions,
pubmed-meshheading:12500029-Indoles,
pubmed-meshheading:12500029-Lung,
pubmed-meshheading:12500029-Male,
pubmed-meshheading:12500029-Maleimides,
pubmed-meshheading:12500029-Nitric Oxide Synthase,
pubmed-meshheading:12500029-Oligopeptides,
pubmed-meshheading:12500029-Peptides, Cyclic,
pubmed-meshheading:12500029-Piperidines,
pubmed-meshheading:12500029-Potassium Channels,
pubmed-meshheading:12500029-Protein Kinase C,
pubmed-meshheading:12500029-Rats,
pubmed-meshheading:12500029-Rats, Wistar,
pubmed-meshheading:12500029-Receptors, Endothelin,
pubmed-meshheading:12500029-Sulfonamides,
pubmed-meshheading:12500029-Vasoconstriction
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pubmed:year |
2003
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pubmed:articleTitle |
ETA, mixed ETA/ETB receptor antagonists, and protein kinase C inhibitor prevent acute hypoxic pulmonary vasoconstriction: influence of potassium channels.
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pubmed:affiliation |
Laboratoire de Physiopathologie et Pharmacologie Cardiovasculaires Expérimentales, Faculté de Médecine, Dijon, France. Francoise.Goirand@u-bourgogne.fr
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pubmed:publicationType |
Journal Article
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