ArticleTheScientificWorldJournal2012
Combined contribution of endothelial relaxing autacoides in the rat femoral artery response to CPCA: an adenosine A2 receptor agonist.
Article in TheScientificWorldJournal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Angiotensin receptor blockers & endothelial dysfunction: Possible correlation & therapeutic implications.The Indian journal of medical research · 2016Review
- Cellular signalling pathways mediating dilation of porcine pial arterioles to adenosine A₂A receptor activation.Cardiovascular research · 2013Article
- Therapeutic approach in the improvement of endothelial dysfunction: the current state of the art.BioMed research international · 2013Review
- Pharmacological analysis of the rat femoral artery response to bradykinin.Scientia pharmaceuticaArticle
- Pioglitazone and Endothelial Dysfunction: Pleiotropic Effects and Possible Therapeutic Implications.Scientia pharmaceuticaReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.