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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1994-8-11
|
| pubmed:abstractText |
The aim of the present study was to elucidate the question of whether cardiomyocytes possess stimulatory adenylyl cyclase-coupled A2-adenosine receptors and whether these receptors modify contractility. In isolated electrically driven ventricular cardiomyocytes from guinea-pig hearts the effects of the A2-adenosine receptor agonist 2-[(p-2-carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamide-adenos ine (CGS 21680C) alone and in the presence of isoprenaline on cAMP content and contractile response were investigated. In addition, we characterized these effects with selective A1- and A2-adenosine receptor antagonists [1,3-dipropyl-8-cyclopentylxanthine, DPCPX and 9-chloro-2-(2-furanyl)-5,6-dihydro-1,2,4-triazolo-(1,5-c)quinazolin++ +-5-imine, CGS 15943A, respectively]. To investigate the signal transduction pathway, the influence of pertussis toxin, known to inhibit signal transducing GTP-binding proteins (Gi/o-proteins), on these effects was studied. CGS 21680C alone and in the presence of isoprenaline increased cAMP content concentration-dependently (0.1 nmol/l-10 mumol/l) to maximally 154% of control and 137% of isoprenaline value, respectively. In the presence of the A1-adenosine receptor antagonist DPCPX (0.3 mumol/l) or after pertussis toxin-pretreatment (18 micrograms/kg i.v. 24-26 h) the cAMP increase was further elevated. The A2-adenosine receptor antagonist CGS 15943A (0.01 mumol/l) abolished these effects, indicating that these effects are mediated by A2-adenosine receptors. The elevation in cAMP content was not accompanied by an increase in contractile response. However, in the presence of isoprenaline CGS 21680C reduced contractile response to 62% of the isoprenaline value. The A1-adenosine receptor antagonist DPCPX abolished the decrease in contractility, whereas the A2-adenosine receptor antagonist CGS 15943A did not effect contractility. Thus the reduction in contractility is mediated via cAMP-decreasing A1-adenosine receptors. The results provide evidence for the coexistence of cAMP-reducing A1- and cAMP-elevating A2-adenosine receptors on ventricular cardiomyocytes. Only stimulation of A1-adenosine receptors leads to a subsequent reduction in contractile response, whereas A2-adenosine receptors do not affect contractility.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1,3-dipropyl-8-cyclopentylxanthine,
http://linkedlifedata.com/resource/pubmed/chemical/2-(4-(2-carboxyethyl)phenethylamino)...,
http://linkedlifedata.com/resource/pubmed/chemical/9-chloro-2-(2-furyl)-(1,2,4)triazolo...,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Phenethylamines,
http://linkedlifedata.com/resource/pubmed/chemical/Quinazolines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Purinergic P1,
http://linkedlifedata.com/resource/pubmed/chemical/Triazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Virulence Factors, Bordetella,
http://linkedlifedata.com/resource/pubmed/chemical/Xanthines
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0022-2828
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
26
|
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
403-14
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:8028023-Adenosine,
pubmed-meshheading:8028023-Adenylate Cyclase,
pubmed-meshheading:8028023-Adenylate Cyclase Toxin,
pubmed-meshheading:8028023-Animals,
pubmed-meshheading:8028023-Cells, Cultured,
pubmed-meshheading:8028023-Cyclic AMP,
pubmed-meshheading:8028023-Drug Interactions,
pubmed-meshheading:8028023-Female,
pubmed-meshheading:8028023-Guinea Pigs,
pubmed-meshheading:8028023-Heart Ventricles,
pubmed-meshheading:8028023-Isoproterenol,
pubmed-meshheading:8028023-Male,
pubmed-meshheading:8028023-Myocardial Contraction,
pubmed-meshheading:8028023-Myocardium,
pubmed-meshheading:8028023-Papillary Muscles,
pubmed-meshheading:8028023-Pertussis Toxin,
pubmed-meshheading:8028023-Phenethylamines,
pubmed-meshheading:8028023-Quinazolines,
pubmed-meshheading:8028023-Receptors, Adrenergic, beta,
pubmed-meshheading:8028023-Receptors, Purinergic P1,
pubmed-meshheading:8028023-Signal Transduction,
pubmed-meshheading:8028023-Triazoles,
pubmed-meshheading:8028023-Virulence Factors, Bordetella,
pubmed-meshheading:8028023-Xanthines
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| pubmed:year |
1994
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| pubmed:articleTitle |
Pharmacological characterization of A2-adenosine receptors in guinea-pig ventricular cardiomyocytes.
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| pubmed:affiliation |
Abteilung Allgemeine Pharmakologie, Universitäts-Krankenhaus Eppendorf, Hamburg, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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