Early afterdepolarization induced by ryanodine in atrial fibers of mouse heart.
The effects of ryanodine on the action potential and induction of early afterdepolarization (EAD) were studied in the atrial fibers of mouse heart. Under treatment with ryanodine, the duration of the action potential (ADP) was prolonged. The percentage of the prolongation of ADP25, APD50 and ADP100 were 83, 49 and 20%, respectively, at a cycle length of 1 sec driving stimulation. As the cycle length was prolonged (from 0.5-10 sec), EAD could be induced in 10 of 16 preparations showing exponential relationship with the cycle length. Tetrodotoxin, lidocaine and nifedipine inhibited the induction of EAD. In 6 preparations in which the EAD was not induced, more than one burst could respond to a single premature stimulation applied in the early phase of repolarization, which was defined as second plateau response. The mechanism of ryanodine-induced EAD has been investigated.
Liu
T F
TF
Department of Biology, Peking University, Beijing, China.
Wang
Z M
ZM
Cheng
Y Z
YZ
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D005260:Female; D006321:Heart / Q000187:drug effects*; D006325:Heart Atria / Q000187:drug effects; D066298:In Vitro Techniques; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D051379:Mice; D009543:Nifedipine / Q000494:pharmacology; D012433:Ryanodine / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology
D012433:Ryanodine; D013779:Tetrodotoxin; D008012:Lidocaine; D009543:Nifedipine