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...

Full description

Saved in:
Bibliographic Details
Published in:TheScientificWorld 2012, Vol.2012 (2012), p.1-7
Main Authors: Topalović, Mirko, Stojanović, Marko, Janković, Radmila, Stojiljković, Milica, Radenković, Miroslav
Format: Article
Language:English
Subjects:
Adenosine - analogs & derivatives
Adenosine - pharmacology
Adenosine A2 Receptor Agonists - pharmacology
Adenosine A2A receptors
Animals
Autacoids - physiology
Channels
Denudation
Endothelial cells
Endothelium
Femoral artery
Femoral Artery - drug effects
Femoral Artery - physiology
Femur
Glibenclamide
Muscle Relaxation - physiology
Na+/K+-exchanging ATPase
Nitric oxide
Nitric-oxide synthase
Ouabain
Pharmacology
Potassium channels
Potassium channels (calcium-gated)
Prostacyclin
Prostaglandin endoperoxide synthase
Rats
Receptors
Receptors, Adenosine A2 - drug effects
Resistance
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:2356-6140
1537-744X
DOI:10.1100/2012/143818