1. Action potentials from sinus venosus and auricle fibers of spontaneously beating frog hearts have been recorded with intracellular electrodes.
2. Sinus fibers show a slow depolarization, the pacemaker potential, during diastole. The amplitude of this potential varies in different parts of the sinus. In some fibers the membrane potential falls by 11 to 15 mv. during diastole and the transition to the upstroke of the action potential is comparatively gradual. In other regions the depolarization develops more slowly and the action potential takes off more abruptly from a higher membrane potential. It is proposed that the fibers showing the largest fall in membrane potential during diastole are the pacemaker fibers of the heart, and that the rest of the preparation is excited by conduction. In auricle fibers the membrane potential is constant during diastole.
3. The maximum diastolic membrane potential and the overshoot of the action potential vary inversely with the amplitude of the pacemaker potential. The highest values were measured in auricle fibers.
4. Stimulation of vagi suppresses the pacemaker potentials. While the heart is arrested the membrane potential of the sinus fibers rises to a level above the maximum diastolic value reached in previous beats. In 28 experiments vagal stimulation increased the membrane potential from an average maximal diastolic value of 55 mv. to a "resting" level of 65.4 mv. The biggest vagal polarization was 23 mv.
5. In contrast to the sinus fibers vagal inhibition does not change the diastolic membrane potential of frog auricle fibers.
6. Vagal stimulation greatly accelerates the repolarization of the action potential and reduces its amplitude. These changes were seen both in the sinus and in auricle fibers stimulated by direct shocks during vagal arrest.
7. The conduction velocity in the sinus venosus of the tortoise is reduced by vagal stimulation. Block of conduction often occurs.
8. In the frog sinus venosus sympathetic stimulation increases the rate of rise of the pacemaker potential, accelerating the beat. The threshold remains unchanged. The rate of rise of the upstroke and the amplitude of the overshoot are increased.
9. The analogies between the vagal inhibition of the heart and the nervous inhibition of other preparations are discussed.