The Antagonizing Mechanism of Acetylcholine on the Atrial Non-Pacemaker Potentials Depressed by Adrenolytics

The depressive effects of adrenolytics on the transmembrane potentials of isolated atria in the intact and reserpinized rabbits have been described in the previous reports (1, 2). The heart which had ceased to beat by the application of the adrenolytics was easily restarted by the addition of adrenaline or noradrenaline. The recovery of the configuration of atrial non-pacemaker potentials by either amine was usually transient and incomplete, though almost full recovery of the repolarization phase of the potentials was observed. In the reserpinized atria, the action potentials depressed by the adrenolytics also restarted and recovered by the addition of acetylcholine except the rate and repolarization phase. The recovering effects of acetylcholine on the restnig potential and the amplitude and depolarization phase of the action potentials were complete and long-lasting. These results suggested that endogenous acetylcholine maintained the depolarization phase, while endogenous noradrenaline regulated the repolarization phase of the transmembrane potentials. The stimulating effects of acetylcholine on the spontaneous contraction of the heart have been reported by many investigators (3-8). These effects are likely to derive from endogenous noradrenaline released by acetylcholine since the stimulating effects of acetylcholine are prevented or blocked by the application of dichlorisoproterenol (DCI) or the full reserpinization (3-5 and 9). However, the restarting effects of acetylcholine on the atria of reserpinized rabbits which had been depressed by the adrenolytics were confirmed in the previous report (2). Moreover, it will be shown that the depressed heart by DCI can be restarted by the addition of acetylcholine but not of catecholamines (10). These evidences suggest that acetylcholine stimulates the heart directly but not indirectly through l endogenously released noradrenaline. On the other hand, the adrenolytics have been reported to affect the effects of acetylcholine in the various structures. Benfey et al. (11) have shown that the adrenolytics block parasympathetic effects of the vagus nerve in the isolated guinea-pig's atria. The blocking effects of di benamine on the pharmacological action of acetylcholine in the aortae and strips of the stomach of rabbits and the isolated auricles of rats have been reported by Furchgott (12). The anti-acetylcholine effects of chlorpromazine have been widely confirmed (13). The present investigations are attempted to correlate depressive effects of the adrenolytics on the transmembrane potentials of the isolated rabbit's atria with endogenous role of acetylcholine.