Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor Agonist

We examined the contribution of endothelial relaxing factors and potassium channels in actions of CPCA, potent adenosine A2 receptor agonist, on isolated intact male rat femoral artery (FA). CPCA produced concentration-dependent relaxation of FA, which was notably, but not completely, reduced after...

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Main Authors: Miroslav Radenković, Marko Stojanović, Radmila Janković, Mirko Topalović, Milica Stojiljković
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:The Scientific World Journal
Online Access:http://dx.doi.org/10.1100/2012/143818
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author Miroslav Radenković
Marko Stojanović
Radmila Janković
Mirko Topalović
Milica Stojiljković
author_facet Miroslav Radenković
Marko Stojanović
Radmila Janković
Mirko Topalović
Milica Stojiljković
author_sort Miroslav Radenković
collection DOAJ
description We examined the contribution of endothelial relaxing factors and potassium channels in actions of CPCA, potent adenosine A2 receptor agonist, on isolated intact male rat femoral artery (FA). CPCA produced concentration-dependent relaxation of FA, which was notably, but not completely, reduced after endothelial denudation. DPCPX, A1 receptor antagonist, had no significant effect, while SCH 58261 (A2A receptor antagonist) notably reduced CPCA-evoked effect. Pharmacological inhibition of nitric oxide synthase or cyclooxygenase comparably reduced CPCA-evoked action, still in a lesser degree than after denudation. In the presence of buffer with high K+ (100  mM), CPCA-produced relaxations were almost abolished. TEA (nonselective KCa blocker), glibenclamide (KATP blocker), Ba++ (KIR blocker), or ouabain (Na+/K+-ATPase inhibitor) did not change CPCA-induced relaxation. Concentration-response curve for CPCA was significantly shifted to the right after the incubation of apamin (SK channel blocker). CPCA produced concentration-dependent relaxation of FA that was partly dependent on endothelial cells. Endothelium-related portion of CPCA-elicited effect was mediated by combined action of endothelial NO, prostacyclin, and EDHF after activation of endothelial A2A receptors. Small conductance KCa channels were involved in this action.
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spelling doaj-art-ee9cdfe246e740b2857c4eccbe7320bc2025-08-20T03:20:43ZengWileyThe Scientific World Journal1537-744X2012-01-01201210.1100/2012/143818143818Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor AgonistMiroslav Radenković0Marko Stojanović1Radmila Janković2Mirko Topalović3Milica Stojiljković4Department of Pharmacology, Clinical Pharmacology and Toxicology, School of Medicine, University of Belgrade, P.O. Box 38, 11129 Belgrade, SerbiaDepartment of Pharmacology, Clinical Pharmacology and Toxicology, School of Medicine, University of Belgrade, P.O. Box 38, 11129 Belgrade, SerbiaInstitute of Pathology, School of Medicine, University of Belgrade, 11000 Belgrade, SerbiaDepartment of Pharmacology, Clinical Pharmacology and Toxicology, School of Medicine, University of Belgrade, P.O. Box 38, 11129 Belgrade, SerbiaDepartment of Pharmacology, Clinical Pharmacology and Toxicology, School of Medicine, University of Belgrade, P.O. Box 38, 11129 Belgrade, SerbiaWe examined the contribution of endothelial relaxing factors and potassium channels in actions of CPCA, potent adenosine A2 receptor agonist, on isolated intact male rat femoral artery (FA). CPCA produced concentration-dependent relaxation of FA, which was notably, but not completely, reduced after endothelial denudation. DPCPX, A1 receptor antagonist, had no significant effect, while SCH 58261 (A2A receptor antagonist) notably reduced CPCA-evoked effect. Pharmacological inhibition of nitric oxide synthase or cyclooxygenase comparably reduced CPCA-evoked action, still in a lesser degree than after denudation. In the presence of buffer with high K+ (100  mM), CPCA-produced relaxations were almost abolished. TEA (nonselective KCa blocker), glibenclamide (KATP blocker), Ba++ (KIR blocker), or ouabain (Na+/K+-ATPase inhibitor) did not change CPCA-induced relaxation. Concentration-response curve for CPCA was significantly shifted to the right after the incubation of apamin (SK channel blocker). CPCA produced concentration-dependent relaxation of FA that was partly dependent on endothelial cells. Endothelium-related portion of CPCA-elicited effect was mediated by combined action of endothelial NO, prostacyclin, and EDHF after activation of endothelial A2A receptors. Small conductance KCa channels were involved in this action.http://dx.doi.org/10.1100/2012/143818
spellingShingle Miroslav Radenković
Marko Stojanović
Radmila Janković
Mirko Topalović
Milica Stojiljković
Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor Agonist
The Scientific World Journal
title Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor Agonist
title_full Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor Agonist
title_fullStr Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor Agonist
title_full_unstemmed Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor Agonist
title_short Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A2 Receptor Agonist
title_sort combined contribution of endothelial relaxing autacoides in the rat femoral artery response to cpca an adenosine a2 receptor agonist
url http://dx.doi.org/10.1100/2012/143818
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