Early afterdepolarization in mouse atrial fibers induced by 3.0 mM K+ and the inhibitory effects of tetrodotoxin and nifedipine.
Early afterdepolarization (EAD) was induced under superfusion of Tyrode solution (K+ = 3.0 mM) at a longer cycle length in mouse atrial fibers. The relationships between the duration and the number of triggered bursts and cycle length were exponential (n = 17). Thus, EAD possesses the property of cycle length dependence. Under a moderate concentration of TTX (4.0 microM) or nifedipine (5.0 microM) treatment, EAD was partially inhibited but maintained cycle length dependence. When a high concentration of the drugs (30 microM and 8.0 microM, respectively) was applied, EAD was abolished at all cycle lengths of driving stimulation. It is suggested that both inward currents (INa and ICa) are involved in the generation of EAD in mouse atrial fibers.
Liu
T F
TF
Department of Biology, Peking University, China.
Cheng
Y Z
YZ
Wei
J H
JH
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D005260:Female; D006321:Heart / Q000294:innervation / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D009412:Nerve Fibers / Q000187:drug effects*; D009467:Neuromuscular Depolarizing Agents; D009543:Nifedipine / Q000494:pharmacology*; D011188:Potassium / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology*
D009467:Neuromuscular Depolarizing Agents; D013779:Tetrodotoxin; D011189:Potassium Chloride; D009543:Nifedipine; D011188:Potassium