ENDOTHELIUM-DEPENDENT RELAXATIONS TO ADENOSINE IN JUVENILE RABBIT PULMONARY-ARTERIES AND VEINS

We studied the actions of adenosine and its analogues 5'-(N-ethylcarbo xamido)-adenosine (NECA) and N-6-cyclohexyladenosine (CHA) in pulmonar y vessels isolated from juvenile rabbits. Pulmonary arteries relaxed i n a concentration-dependent fashion to all three compounds. Pretreatme nt with the methylxanthine 8-p-sulfophenyltheophylline shifted the con centration-response curves to adenosine and NECA rightward, indicating that the vasodilator effects were mediated by the adenosine receptor. The order of potency of adenosine coumpounds was NECA > adenosine > C HA, indicating that the A(2)-receptor mediates relaxations to adenosin e in rabbit pulmonary arteries. Endothelium rubbing attenuated relaxat ions to adenosine at concentrations of less than or equal to 3 x 10(-7 ) M and to all NECA concentrations. Inhibition of nitric oxide synthas e with NG-nitro-L-arginine (L-NNA) similarly attenuated relaxations at concentrations of less than or equal to 3 x 10(-7) M for adenosine an d less than or equal to 3 x 10(-8) M for NECA. With the use of the sam e methods, a substantial endothelial contribution was additionally obs erved in pulmonary veins to the vasodilator effects of NECA. We conclu de that adenosine, and the more specific A(2)-receptor agonist NECA, d ilate pulmonary arteries and veins isolated from young rabbits via a m echanism that is partially dependent on endothelium-derived nitric oxi de.