Interaction of the adenosine A1 receptor agonist N6-cyclopentyladenosine and κ-opioid receptors in rat spinal cord nociceptive reflexes

2014 ◽  
Vol 25 (8) ◽  
pp. 741-749 ◽  
Author(s):  
Guillermo A. Ramos-Zepeda ◽  
Carlos Herrero-Zorita ◽  
Juan F. Herrero
Keyword(s):  
Spinal Cord ◽  
Opioid Receptors ◽  
Receptor Agonist ◽  
Adenosine A1 Receptor ◽  
Rat Spinal Cord ◽  
Adenosine A1 ◽  
Nociceptive Reflexes ◽  
A1 Receptor

Adenosine improves recovery of postischemic myocardial function via an adenosine A1 receptor mechanism

1992 ◽  
Vol 263 (5) ◽  
pp. H1460-H1465 ◽  
Author(s):  
R. D. Lasley ◽  
R. M. Mentzer
Keyword(s):  
Receptor Agonist ◽  
Myocardial Function ◽  
Left Ventricular ◽  
Adenosine A1 Receptor ◽  
Extracellular Adenosine ◽  
Adenosine A2 Receptor ◽  
Rat Hearts ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
A2 Receptors

The effects of adenosine in the nonischemic heart have been shown to be mediated via its binding to extracellular adenosine A1 and A2 receptors located predominantly on myocytes and endothelial cells, respectively. We tested the hypothesis that the beneficial effect of adenosine on postischemic myocardial function is mediated via an adenosine A1 receptor mechanism. Isolated rat hearts perfused at constant pressure (85 cmH2O) were subjected to 30 min of global no-flow ischemia (37 degrees C) and 45 min of reperfusion. Hearts treated with adenosine (100 microM) and the adenosine A1 receptor agonist N6-cyclohexyladenosine (CHA; 0.25 microM) recovered 72 +/- 4 and 70 +/- 4% of preischemic left ventricular developed pressures (LVDP), respectively, after 45 min of reperfusion compared with untreated hearts (54 +/- 3% of preischemic LVDP). Adenosine and CHA hearts exhibited greater myocardial ATP contents than control hearts after 10 min of ischemia, but there were no differences in tissue ATP levels after 30 min of ischemia. In contrast, hearts treated with the adenosine A2 receptor agonist phenylaminoadenosine (0.25 microM) failed to demonstrate improved postischemic function (52 +/- 5%). The addition of the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine blocked the cardioprotective effect of adenosine (57 +/- 4%). These results suggest that adenosine enhances postischemic myocardial function via an A1 receptor mechanism.

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