Sympathetic nerve stimulation and applied transmitters on the sinus venosus of the toad.

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Abstract
1. The effect of sympathetic nerve stimulation on pacemaker cells of the isolated sinus venosus of the toad, Bufo marinus, were examined using intracellular recording techniques. 2. Train of stimuli applied to the sympathetic outflow led to a two‐component increase in heart rate. Shortly after the onset of stimulation the rate of discharge of pacemaker action potentials increased. After the end of the train of stimuli, the heart rate fell and then again increased to remain high for several minutes. 3. During the early tachycardia, the peak diastolic potential was reduced and the rate of diastolic depolarization increased. During the late tachycardia, the peak diastolic potential and rate of diastolic depolarization were increased; both the amplitude and the rate of repolarization of the action potentials were increased. 4. When membrane potential recordings were made from sinus venosus cells in which beating had been abolished by adding the organic calcium antagonist nicardipine, sympathetic nerve stimulation caused membrane depolarization. 5. The responses to sympathetic nerve stimulation, recorded from beating or arrested hearts, were abolished by bretylium but persisted in the presence of a number of beta‐adrenoceptor antagonists. 6. Bath‐applied adrenaline caused a tachycardia which was associated with a large increase in the amplitudes of pacemaker action potentials. These effects were largely mediated by the activation of beta 2‐adrenoceptors. 7. In the presence of high concentrations of beta‐adrenoceptor antagonists, applied adrenaline produced membrane potential changes that although slower in time course were similar to those produced by sympathetic nerve stimulation. 8. Many aspects of the responses to nerve stimulation could be mimicked by applied ATP. 9. The early phase of sympathetic tachycardia was abolished after P2‐purinoceptor desensitization; this phase was also inhibited by dihydroergotamine. 10. The results are discussed in relation to the idea that sympathetic nerve stimulation causes the early tachycardia by increasing inward current flow during diastole, a response involving activation of specialized adrenoceptors and perhaps ATP receptors.