Action of adenine derivatives on experimental atrial flutter in the canine heart

We have studied the effects of adenosine (Ado) and adenosine derivatives on an experimental atrial flutter (AFL) in the canine heart. Moreover, we have assessed these adenine derivatives on some electrophysiological parameters (the conduction time and functional refractory period) of the posterior internodal pathway (PIP) and of the ordinary atrial myocardium (OAM). The adenosine derivatives assessed were adenosine 5'-monophosphate (AMP), adenosine 3' 5'-monophosphate (cAMP) and adenosine 5'-triphosphate (ATP). Ado, AMP, and cAMP transformed the atrial flutter into a short episode of atrial fibrillation that terminated spontaneously to sinus rhythm. This effect was prevented by previous blockade of A1 purinergic receptors with aminophylline, but not by parasympathectomy (vagotomy and atropine). ATP also suppressed the AFL, but in this case, sinus rhythm was achieved without an intermediate episode of atrial fibrillation, and the effect of ATP was not prevented by A1 purinergic blockade. Ado, AMP and cAMP extended the functional refractory period measured in the PIP, but reduced this parameter in the OAM (p < 0.01). The different response of atrial tissues to the adenosine and its monophosphate derivatives was not elicited by ATP. This derivative caused a prolongation of FRP on both atrial tissues PIP and OAM (p < 0.05). The changes produced by Ado and its monophosphate derivatives on FRP was blocked by aminophylline. The effect of adenine derivatives on AFL may be explained by the dispersion of refractoriness created as a result of the heterogeneous response of atrial tissues to these agents. Our results support the hypothesis of an agonistic action of adenine derivatives on atrial purinergic receptors.