Observation on functional pacemaker cell were intracellularly made in several experimental solutions in which Phentolamine, Propranolol and others were contained. In all experiments a frogs heart was excised together with vagosympathetic nerve. The ventricle and large part of the auricles were cut away. This nerve-sinus preparation was perfused with Ringer's solution saturated with 95 %O2+5% CO2.
The following results were obtained.
1) α-blockade (Phentolamine) increased the slope of diastolic depolarization and also raised the threshold potential, therefore gradually caused slowing of the pulse rate. The ratio of prepotential to pacemaker potential was very increased. Accordingly a latent potential often changed to a true potential.
In concentration from 10-3 to 10-4 M, the movement of contraction disappeared in spite of the presence of action potential.
It can therefore be presumed that E-C coupling will be blocked here.
2) β-blckade (Propranolol) decreased the slope of diastolic depolarization. It developed a stagnant step between 4 and 0 phase and inhibited firing at the law level of threshold potential.
3) Furthermore, some factors which decreased or increased the prepotential were classified. Ach, vagosympathetic nerve stimulation and Propranolol decreased it. On the contrary, Isoproterenol, Atrope and Phentolamine increased it.
From these results it can also be presumed that the pacemaker potential will be divided into P and Q cell potential.
The former makes the prepotential only and the latter makes conduction and contraction potential.
In order to certificate this theory the further investigation between nerve terminal and pacemaker cell will be needed.
