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1 Department of Pharmacology, Faculty of Medicine, Kyoto University, Kyoto, Japan
Vagus-atrial preparations isolated from rabbits were used. Transmembrane potentials were recorded from sinoatrial (S-A) nodal pacemaker fibers in the steady state and under stimulation of extracardiac vagus nerves. In preparations from animals pretreated with reserpine the S-A nodal rate was slowed compared with that in normal preparations, whereas the negative chronotropic response to vagal stimulation and the membrane potential of the S-A nodal fiber did not differ. The pretreatment with reserpine increased the incidence of bradycardia at excess [Ca++]0 but did not affect the other parameters measured in response to various [Ca++]0 . A Na+ deficiency decreased the S-A nodal electrical activity, but increased the negative and positive chronotropic response to vagal stimulation. The positive response obtained at low [Na+]0 was not antagonized by pretreatment of animals with reserpine and application of propranolol, but it was antagonized by atropine sulfate. In preparations in which the S-A nodal activity had been abolished at low [Na+]0, cholinergic stimulation induced marked hyperpolarization followed by a transient recovery of the activity. The recovery was not inhibited either by pretreatment with reserpine or by application of propranolol. Atropine sulfate markedly decreased the hyperpolarization but not the reinitiating response within 10 min. From these results it was proposed that endogenous acetylcholine possessed cardio-excitatory action which was independent of the release of cardiac catecholamines but atropine-resistant.
Submitted on August 15, 1967
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