Vagal and Sympathetic Effects on the Pacemaker Fibers in the Sinus Venosus of the Heart

Abstract

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.

Influence of sodium ions on the membrane potential of the sino‐atrial node in response to sympathetic nerve stimulation

“…Membrane effects of adrenaline are presumed to be due to an increase in permeability to Na+ during diastole (Trautwein, 1963). Observations of an increased size of the over-shoot and an increased upstroke velocity further suggest that stimulation of vagosympathetic nerves in isolated frog hearts (Hutter & Trautwein, 1956) and application of adrenaline to sheep Purkinje fibres (Otsuka, 1958) increase the permeability to Na+ upon depolarization. However, no evidence of the increase in the Na+ permeability during systole is obtained from isolated rabbit atria in which post-ganglionic sympathetic nerves are stimulated electrically (Toda & Shimamoto, 1968).…”

Synaptic delay in the heart: an ionophoretic study.

“…Other workers have reported minimum latencies of 100-200 msec for the vagal inhibitory effect in intact hearts (Brown & Eccles, 1934) and both inotropic and chronotropic actions evoked by sympathetic nerves are reported to have latencies of several seconds (Amory & West, 1962;Toda & Shimamoto, 1968). In amphibian hearts, vagal (del Castillo & Katz, 1955) and sympathetic (Stewart, 1892;Hutter & Trautwein, 1956) actions are even slower than in mammals.…”

Electrophysiological Analysis of the Gastric Smooth Muscle Fiber of Guinea-pig and Rabbit

“…From the experimental results with TTX, low Ca/Mg ratio and chronaxie for generation of ijp, it is most likely that the slow hyperpolarizing response, referred the preparation which had contracted spontaneously, indicating that adrenalin would act on muscle fiber in two ways; one is the hyperpolarization of cell mem brane, and the other might be augmentation of pacemarker potential, like that in heart muscle (Hutter and Trautwein 1956). Further experiment seems to be needed for elucidating the nature of effect of adrenalin.…”

“…Therefore, the difference of the latencies in d and e may be explained by that of the diffusion time of transmitter released from nerve terminal. This explanation made sure the possibility that the receptor for generating ejp may contact loosely with the nerve terminal which releases the mediator, not as neuromuscular junc tion, but as inhibitory potential evoked by vagal stimulation on heart muscle (Hutter and Trautwein 1956;Satow 1968). By repetitive stimulations, ejps were easily summated up to the threshold level from which the spike potential fired in many cases.…”