Revisiting the ionic mechanisms of early afterdepolarizations in cardiomyocytes: predominant by Ca waves or Ca currents?. Zhao, Z., Wen, H., Fefelova, N., Allen, C., Baba, A., Matsuda, T., & Xie, L. American journal of physiology. Heart and circulatory physiology, 302(8):H1636-44, 4, 2012.
Revisiting the ionic mechanisms of early afterdepolarizations in cardiomyocytes: predominant by Ca waves or Ca currents? [link]Website  abstract   bibtex   
Early afterdepolarizations (EADs) have been implicated in severe cardiac arrhythmias and sudden cardiac deaths. However, the mechanism(s) for EAD genesis, especially regarding the relative contribution of Ca(2+) wave (CaW) vs. L-type Ca current (I(Ca,L)), still remains controversial. In the present study, we simultaneously recorded action potentials (APs) and intracellular Ca(2+) images in isolated rabbit ventricular myocytes and systematically compared the properties of EADs in the following two pharmacological models: 1) hydrogen peroxide (H(2)O(2); 200 μM); and 2) isoproterenol (100 nM) and BayK 8644 (50 nM) (Iso + BayK). We assessed the rate dependency of EADs, the temporal relationship between EADs and corresponding CaWs, the distribution of EADs over voltage, and the effects of blockers of I(Ca,L), Na/Ca exchangers, and ryanodine receptors. The most convincing evidence came from the AP-clamp experiment, in which the cell membrane clamp was switched from current clamp to voltage clamp using a normal AP waveform without EAD; CaWs disappeared in the H(2)O(2) model, but persisted in the Iso + BayK model. We postulate that, although CaWs and reactivation of I(Ca,L) may act synergistically in either case, reactivation of I(Ca,L) plays a predominant role in EAD genesis under oxidative stress (H(2)O(2) model), while spontaneous CaWs are a predominant cause for EADs under Ca(2+) overload condition (Iso + BayK model).
@article{
 title = {Revisiting the ionic mechanisms of early afterdepolarizations in cardiomyocytes: predominant by Ca waves or Ca currents?},
 type = {article},
 year = {2012},
 identifiers = {[object Object]},
 keywords = {Action Potentials,Action Potentials: drug effects,Adrenergic beta-Agonists,Adrenergic beta-Agonists: pharmacology,Aniline Compounds,Aniline Compounds: pharmacology,Animals,Calcium Channel Agonists,Calcium Channel Agonists: pharmacology,Calcium Channel Blockers,Calcium Channel Blockers: pharmacology,Calcium Channels,Calcium Channels: physiology,Calcium Signaling,Calcium Signaling: physiology,Electrophysiological Phenomena,Electrophysiological Phenomena: physiology,Heart Ventricles,Homeodomain Proteins,Hydrogen Peroxide,Hydrogen Peroxide: pharmacology,Isoproterenol,Isoproterenol: pharmacology,Kinetics,Myocytes, Cardiac,Myocytes, Cardiac: physiology,Patch-Clamp Techniques,Phenyl Ethers,Phenyl Ethers: pharmacology,Rabbits,Ryanodine,Ryanodine Receptor Calcium Release Channel,Ryanodine Receptor Calcium Release Channel: drug e,Ryanodine: pharmacology,Sarcoplasmic Reticulum,Sarcoplasmic Reticulum: drug effects,Sarcoplasmic Reticulum: physiology,Sodium-Calcium Exchanger,Sodium-Calcium Exchanger: antagonists & inhibitors},
 pages = {H1636-44},
 volume = {302},
 websites = {http://ajpheart.physiology.org/cgi/content/abstract/ajpheart.00742.2011v1},
 month = {4},
 day = {15},
 id = {3eecd932-02f7-350c-866a-7a3042e68cd6},
 created = {2012-09-16T13:29:41.000Z},
 accessed = {2012-09-16},
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 profile_id = {409abeb6-746c-3cb1-be13-1f6c69a35474},
 last_modified = {2017-03-15T18:44:14.327Z},
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 abstract = {Early afterdepolarizations (EADs) have been implicated in severe cardiac arrhythmias and sudden cardiac deaths. However, the mechanism(s) for EAD genesis, especially regarding the relative contribution of Ca(2+) wave (CaW) vs. L-type Ca current (I(Ca,L)), still remains controversial. In the present study, we simultaneously recorded action potentials (APs) and intracellular Ca(2+) images in isolated rabbit ventricular myocytes and systematically compared the properties of EADs in the following two pharmacological models: 1) hydrogen peroxide (H(2)O(2); 200 μM); and 2) isoproterenol (100 nM) and BayK 8644 (50 nM) (Iso + BayK). We assessed the rate dependency of EADs, the temporal relationship between EADs and corresponding CaWs, the distribution of EADs over voltage, and the effects of blockers of I(Ca,L), Na/Ca exchangers, and ryanodine receptors. The most convincing evidence came from the AP-clamp experiment, in which the cell membrane clamp was switched from current clamp to voltage clamp using a normal AP waveform without EAD; CaWs disappeared in the H(2)O(2) model, but persisted in the Iso + BayK model. We postulate that, although CaWs and reactivation of I(Ca,L) may act synergistically in either case, reactivation of I(Ca,L) plays a predominant role in EAD genesis under oxidative stress (H(2)O(2) model), while spontaneous CaWs are a predominant cause for EADs under Ca(2+) overload condition (Iso + BayK model).},
 bibtype = {article},
 author = {Zhao, Zhenghang and Wen, Hairuo and Fefelova, Nadezhda and Allen, Charelle and Baba, Akemichi and Matsuda, Toshio and Xie, Lai-Hua},
 journal = {American journal of physiology. Heart and circulatory physiology},
 number = {8}
}
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