THE MODE OF ACTION OF RESERPINE ON THE TRANSMEMBRANE POTENTIAL OF RABBIT'S ATRIUM IN VITRO

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It has been shown in the previous report (1) that reserpine depressed the transmembrane potentials of the sinoatrial pacemaker and non-pacemaker atrial fibers of the isolated rabbit's atrium in rhythm and in configuration. Within 2 hours after the application of reserpine above the concentration of 10-5 the action potentials disappeared totally. Adrenaline or noradrenaline antagonized the depressive effect of reserpine on the action potential, and the administration of either amine restarted the rhythmic action potentials. The mode of action of reserpine on the action potential was discussed being derived from release and depletion of noradrenaline in the atrial fibers. The content of noradrenaline in the spontaneously beating atrium of guinea-pig which had been immersed in oxygenated Tyrode's solution at 29°C decreased gradually (2). Using the isolated atrium of rabbit, Matsuo (3) showed that the concentration of 10-5 of reserpine resulted in the depletion of about 30 to 40% of the amine at 2 hours after the administration in contrast to the slight decrease (5 to 10%) of control amine content. On the other hand, despite of deprivation of about 90% of noradrenaline in the heart of various animals in response to 0.1 to 1.0 mg/kg of reserpine administered intravenously (4-8), the heart continued its rhythmic contraction in situ. This difference of action of reserpine on the heart between in vivo and in vitro suggests some mechanisms of action of reserpine other than the liberation of noradrenaline from the heart in vitro or some compensatory mechanisms of heart in situ to maintain the rhythmic contraction against the extreme depletion of noradrenaline. Plummer et al. (9) and Krayer et al. (10) showed that reserpine increased the heart rate in the heart-lung preparation of dog. The latter authors postulated that the increase of the heart rate at the early phase of reserpine action was attributable to the increased liberation of noradrenaline into the perfusion fluid from the heart. However, the atrial preparation of rabbit showed only a decrease of rate of the action potential or the rhythmic contraction in response to a wide range of reserpine concentration (1, 11). The depression of the atrial rate might be caused by the non-specific antiaccelerator effect of reserpine, originally described by Krayer and Fuentes (10). Pepeu et al. (2) showed that the pretreatment of the atrium of guinea-pig with iproniazid reversed the noradrenaline depleting action of reserpine in vitro, but the similar treatment with phenylisopropyl hydrazine did not reverse the reserpine effect. Tachi (personal communication) and the author showed that the pretreatment of rabbit with iproniazid or SKF-385 (2-phenylcyclopropylamine) did not antagonize the depressive effect of reserpine on the atrium in vitro, though the pretreatment of these monoamine oxidase inhibitors slightly but significantly prolonged the course of the reserpine action. Assaying the content of noradrenaline in these atria, Matsuo (3) confirmed the reversal of reserpine action by iproniazid and SKF-385. In this experiment the effects of reserpine were investigated on the transmembrane potentials of atrium of rabbit pretreated with reserpine or SKF-385 and those of the normal atrium which was electrically driven after the excision of its sinoatrial node.
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THE MODE OF ACTION OF RESERPINE ON THE TRANSMEMBRANE POTENTIAL OF RABBIT'S ATRIUM <I>IN VITRO</I>

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