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SUMMARY. Adenosine is known to cause atrioventricular block by slowing conduction through the atrioventricular node, thereby lengthening the atria to His (A-H) interval. To test the hypothesis that the increase in atrioventricular conduction delay produced by adenosine is mediated at an extracellular site, the efficacy of nucleoside transport inhibitors in preventing cellular adenosine uptake was correlated with their ability to potentiate the atrioventricular block and prolong the A- H interval. The antagonism of aminophylline and adenosine also was examined. Since methylxan- thines are known to inhibit cyclic nucleotide phosphodiesterase, to release catecholamines from nerve terminals, and to block adenosine receptors, it was determined whether the ability of aminophylline to reverse the adenosine-induced prolongation of the atrial-His interval and atrioven- tricular block was associated with an increase in myocardial cyclic AMP and/or release of norepi- nephrine. The atrial-His conduction time and adenosine uptake and release were determined in isolated perfused guinea pig and rat hearts. The nucleoside transport inhibitors dipyridamole, nitrobenzylthioinosine, and diazepam caused a dose-dependent decrease in the uptake of 14C- adenosine. Nitrobenzylthioinosine was the most and diazepam the least effective in blocking adenosine uptake. Dipyridamole (5 X 10~6 M) inhibited uptake by 97% and increased adenosine levels in the perfusate. These effects were strongly correlated with a potentiation of adenosine- induced atrial-His prolongation (r = 0.99). The oligonucleotide, adenyl (3'-5')9-adenosine, an agent restricted to the extracellular space as a result of its large molecular size, was found to be 1.8 times more potent per mole than free adenosine. 2'-Deoxyadenosine and N 6

circulation research

Extracellular action of adenosine and the antagonism by aminophylline on the atrioventricular conduction of isolated perfused guinea pig and rat hearts.