MODIFICATIONS OF THE VAGAL EFFECT ON THE HEART AND THE CARDIAC METABOLISM BY RESERPINE IN VITRO

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The previous reports from this laboratory (1-4) have shown that reserpine in a concentration of 10-5 g/ml results in a decrease in the amplitude and prolongation of depolarization and repolarization phases of transmembrane action potential and sometimes an arrest of rhythmic contraction in the isolated rabbit atria. The finding that noradrenaline restarts the atrial beat which has been arrested by reserpine led us to the assumption that endogenous noradrenaline may play an important role in the intrinsic rhythmicity of the heart. However, there has been presented evidence against this assumption (5, 6). The arrested atria can be restarted by noradrenaline without significant increase in the level of tissue noradrenaline. By contrast, the atria from the rabbit pretreated with reserpine and depleted of noradrenaline continue to contract long after isolation. Consequently, it has been postulated that the cardiac inhibitory effects of reserpine in vitro do not derive from a decrease in the amount of endogenous catecholamines but from some direct action of unknown mechanism (4). In the course of experiments studying the effects of adrenergic drugs on the atrial response to stimulation of the vagus nerve, Toda et al. (7) have found that a deficiency of oxygen supply results in a potentiation of the vagal response without modifying acetylcholine response and this is similar to that of reserpine. Reserpine reduces oxygen consumption of the isolated rabbit intestine (8) and the rat brain homogenate as well as liver and kidney slices (9). The present experiments were designed to ascertain whether a close relationship exists between the cardiac inhibitory effect and the depression of tissue respiration following reserpine in vitro.
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MODIFICATIONS OF THE VAGAL EFFECT ON THE HEART AND THE CARDIAC METABOLISM BY RESERPINE <I>IN VITRO</I>

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