The effect of quinidine (class 1 agent) and verapamil (class 4 agent) on the adenosine-induced changes in the electrical and mechanical activity of the left atrial myocardium of guinea-pig was studied. Adenosine alone shortened the action potential duration, slightly hyperpolarized the membrane and increased the V̇(max) as well as induced a negative inotropic effect. Quinidine, a membrane-stabilizing drug, prolonged the action potential duration, decreased the V̇(max), and increased the contractile force, i.e. diminished the electrical and mechanical changes in the atria treated with adenosine. These effects became more pronounced in the presence of aminophylline, a P1-purinoceptor blocker. In contrast, verapamil, a Ca-channel blocker, enhanced the adenosine-induced shortening in the early repolarization phase of the action potential, and the negative inotropic effect. This action of verapamil could be attenuated with aminophylline. The results suggest that adenosine can influence the effect of antiarrhythmics compounds and vice versa, and that the action of adenosine is possibly mediated via interaction with an extracellular P1-purinoceptor.
|Number of pages||13|
|Journal||Archives internationales de pharmacodynamie et de therapie|
|Publication status||Published - Jan 1 1986|
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