Source:http://linkedlifedata.com/resource/pubmed/id/10938247
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2000-8-31
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pubmed:abstractText |
We characterize herein the impact of myocardial nitric oxide (NO) synthesis on the inotropic response to two cardioactive peptides, endothelin-1 (ET-1) and adrenomedullin (AM). In the isolated perfused rat heart preparation, intracoronary infusion of AM (0.03 and 1 nmol/l) and ET-1 (0.08 and 1 nmol/l) for 30 min induced a dose-dependent, gradual increase in developed tension, the maximal responses being equal. Inhibition of myocardial NO synthase (NOS) by N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 micromol/l) enhanced the inotropic response to ET-1 at a concentration of 1 nmol/l; meanwhile, the effect of AM was not augmented significantly. The inotropic response to simultaneous administration of low, equipotent doses of AM (0.03 nmol/l) and ET-1 (0.08 nmol/l) was significantly smaller than that of either peptide alone. This depressed response was more than overcome by concomitant administration of L-NAME. In conclusion, this study reveals that the maximal inotropic response to ET-1 can be augmented by inhibition of myocardial NOS, whereas it has only a minor impact on the effect of AM. The inotropic response to combined administration of low doses of AM and ET-1 is substantially suppressed by endogenous NO, whereas the individual effects of the peptides at these doses are not the subject of secondary modulation by NO.
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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/Adrenomedullin,
http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0363-6119
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
279
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
R569-75
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10938247-Adrenomedullin,
pubmed-meshheading:10938247-Animals,
pubmed-meshheading:10938247-Drug Combinations,
pubmed-meshheading:10938247-Drug Synergism,
pubmed-meshheading:10938247-Endothelin-1,
pubmed-meshheading:10938247-Enzyme Inhibitors,
pubmed-meshheading:10938247-Hemodynamics,
pubmed-meshheading:10938247-Male,
pubmed-meshheading:10938247-Myocardial Contraction,
pubmed-meshheading:10938247-Myocardium,
pubmed-meshheading:10938247-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:10938247-Nitric Oxide,
pubmed-meshheading:10938247-Nitric Oxide Synthase,
pubmed-meshheading:10938247-Peptides,
pubmed-meshheading:10938247-Rats,
pubmed-meshheading:10938247-Rats, Sprague-Dawley
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pubmed:year |
2000
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pubmed:articleTitle |
Impact of NO on ET-1- and AM-induced inotropic responses: potentiation by combined administration.
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pubmed:affiliation |
Department of Pharmacology and Toxicology, Biocenter Oulu, University of Oulu, Finland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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