In anesthetized rats, intravenous injection of 1-(1-pyrrolidinylmethyl)-2-naphthol (TPY-beta, 0.1-1 mg/kg) induced a transient (less than 1 min) decrease in arterial blood pressure and heart rate (acute responses) followed by a delayed and sustained (greater than 10 min) bradycardic response. The electrophysiological mechanisms responsible for the bradycardic effect of TPY-beta were studied in sinoatrial tissues isolated from guinea-pig hearts. Transmembrane action potential (AP) and twitch force of atrial tissues were recorded with the conventional microelectrode techniques. In sinoatrial pacemakers active spontaneously in 4 mM [K]o Tyrode solution, TPY-beta (3-100 microM) depressed the diastolic slope and the rate of spontaneous discharges. When the non-automatic atrial tissues were driven at a fixed rate, TPY-beta (10-100 microM) inhibited the upstroke velocity of phase-0 depolarization and prolonged AP duration. In atrial fibers depolarized in high [K]o (24 mM), TPY-beta depressed the phase-0 upstroke of slow response AP and the twitch force in a concentration-dependent manner. The present results indicate that TPY-beta induced direct negative chronotropic and inotropic effects on guinea-pig atrial pacemakers and myocardial fibers. The underlying mechanisms involve a general inhibition of transmembrane of Ca, K and Na ion fluxes.