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Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist
We examined the contribution of endothelial relaxing factors and potassium channels in actions of CPCA, potent adenosine A(2) receptor agonist, on isolated intact male rat femoral artery (FA). CPCA produced concentration-dependent relaxation of FA, which was notably, but not completely, reduced afte...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Scientific World Journal
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3349095/ https://www.ncbi.nlm.nih.gov/pubmed/22619589 http://dx.doi.org/10.1100/2012/143818 |
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author | Radenković, Miroslav Stojanović, Marko Janković, Radmila Topalović, Mirko Stojiljković, Milica |
author_facet | Radenković, Miroslav Stojanović, Marko Janković, Radmila Topalović, Mirko Stojiljković, Milica |
author_sort | Radenković, Miroslav |
collection | PubMed |
description | We examined the contribution of endothelial relaxing factors and potassium channels in actions of CPCA, potent adenosine A(2) 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, A(1) receptor antagonist, had no significant effect, while SCH 58261 (A(2A) 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 K(Ca) blocker), glibenclamide (K(ATP) blocker), Ba(++) (K(IR) 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 A(2A) receptors. Small conductance K(Ca) channels were involved in this action. |
format | Online Article Text |
id | pubmed-3349095 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | The Scientific World Journal |
record_format | MEDLINE/PubMed |
spelling | pubmed-33490952012-05-22 Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist Radenković, Miroslav Stojanović, Marko Janković, Radmila Topalović, Mirko Stojiljković, Milica ScientificWorldJournal Research Article We examined the contribution of endothelial relaxing factors and potassium channels in actions of CPCA, potent adenosine A(2) 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, A(1) receptor antagonist, had no significant effect, while SCH 58261 (A(2A) 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 K(Ca) blocker), glibenclamide (K(ATP) blocker), Ba(++) (K(IR) 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 A(2A) receptors. Small conductance K(Ca) channels were involved in this action. The Scientific World Journal 2012-04-19 /pmc/articles/PMC3349095/ /pubmed/22619589 http://dx.doi.org/10.1100/2012/143818 Text en Copyright © 2012 Miroslav Radenković et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Radenković, Miroslav Stojanović, Marko Janković, Radmila Topalović, Mirko Stojiljković, Milica Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist |
title | Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist |
title_full | Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist |
title_fullStr | Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist |
title_full_unstemmed | Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist |
title_short | Combined Contribution of Endothelial Relaxing Autacoides in the Rat Femoral Artery Response to CPCA: An Adenosine A(2) Receptor Agonist |
title_sort | combined contribution of endothelial relaxing autacoides in the rat femoral artery response to cpca: an adenosine a(2) receptor agonist |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3349095/ https://www.ncbi.nlm.nih.gov/pubmed/22619589 http://dx.doi.org/10.1100/2012/143818 |
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