Manganese ions suppressed AV nodal cell activity while tetrodotoxin rendered atrial and His bundle fibers inexcitable without preventing AV nodal potentials, suggesting a slow ionic channel mechanism.
Demonstrates that AV nodal action potentials in isolated rabbit hearts likely depend on a slow ionic channel, based on their resistance to TTX and sensitivity to Mn2+.
In the isolated rabbit heart, it was shown that (1) manganese ions (Mn 2+ ) (2-4 m M ) suppressed the activity of atrioventricular (AV) nodal cells located in the AN, N, and NH regions without preventing regenerative responses in atrial or His bundle fibers when these fibers were directly stimulated, (2) tetrodotoxin (TTX) in concentrations of 5 x 10 -6 g/ml Tyrode's solution rendered atrial and His bundle fibers inexcitable without preventing AV nodal potentials of automatic origin and without affecting the rate of rise of cells located in the N region, and (3) in the presence of TTX (5 x l0 -6 g/ml of Tyrode's solution) the addition of epinephrine (2 µg/ml solution) restored atrial activity. It was concluded that the different effects of Mn 2+ and TTX on AV nodal action potentials is consistent with the postulate, made by Rougier et al. (8) and Vassort et al. (9) for frog atrial fibers treated with TTX, that AV nodal action potentials probably result from the operation of a slow ionic channel.
Zipes et al. (1973) studied Electrophysiology of isolated rabbit hearts. Manganese ions (Mn2+) and Tetrodotoxin (TTX) was evaluated on Atrioventricular nodal transmembrane potentials. Manganese ions suppressed AV nodal cell activity while tetrodotoxin rendered atrial and His bundle fibers inexcitable without preventing AV nodal potentials, suggesting a slow ionic channel mechanism.