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Role of take-off potential and second plateau response in generation of early afterdepolarization in arterial fibers of mouse heart.

Take-off potentials (TOPs) of triggered bursts were studied on aconitine- 3.0 mM K+ and quinidine-induced early afterdepolarization (EADs) in mice atrial fibers. TOPs varied from -40 to -66 mV (-53.4 +/- 6.4 mV, n = 14) depending on the cycle length of stimulation. TOPs were cycle length-dependent and the relationship between TOP and cycle length was exponential. Before the generation of EAD, a second plateau appeared following the rapid repolarization phase of action potential (AP). In some preparations, EAD could not be induced, especially at a shorter cycle length, leaving a definite second plateau following the AP under treatment with effective agents. By application of a premature stimulation on the second plateau, only one burst could be observed. However, two or more bursts could be induced when a stimulation was applied on the rapid repolarization phase at -50 +/- 6 mV (n = 17) level. We defined this phenomenon as "second plateau response" which was studied in the present work under treatment with quinidine (4 cases), 3.0 mM K+ (4), ryanodine (6) and Bay K 8644 (3). The second plateau response was abolished by tetrodotoxin (1.0 microM), nifedipine (2.0 microM) or rapid driving. All of these were similar to the properties of the EAD. It is suggested that the second plateau response may be taken as an indicator of the capability of the EAD generation in myocardiac cells.