Abstract
1. The effects of sympathetic nerve stimulation on membrane potential and on the intracellular concentration of calcium ions, [Ca2+]i, were recorded concurrently from the sinus venosus of the toad, Bufo marinus, in preparations where beating had been abolished by adding an organic calcium antagonist to the physiological saline. In a separate set of experiments the effects of sympathetic nerve stimulation on force production were examined. 2. Stimulation of the sympathetic nerves caused a membrane depolarization and a simultaneous increase in [Ca2+]i. Both responses were reduced by dihydroergotamine (20 microM). 3. The membrane depolarization and increase in [Ca2+]i evoked by sympathetic nerve stimulation were abolished by ryanodine (10 microM), or caffeine (3 mM). The effects of caffeine, but not those of ryanodine, were fully reversible. 4. Although the Ca(2+)-ATPase inhibitor thapsigargin (30 microM) itself had little effect on the responses to sympathetic nerve stimulation, in its presence caffeine (3 mM) irreversibly abolished the responses. 5. In the presence of nifedipine (10 microM), sympathetic nerve stimulation caused contractions of the sinus venosus. These responses were abolished by either ryanodine (10 microM) or caffeine (3 mM). 6. The results suggest that neuronally released transmitter activates a complex biochemical pathway which triggers the release of Ca2+ from internal stores.