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• W2218211815 endingPage "H2178" @default.
• W2218211815 startingPage "H2168" @default.
• W2218211815 abstract "Early afterdepolarizations (EAD) caused by L-type Ca 2+ current ( I Ca,L ) are thought to initiate long Q-T arrhythmias, but the role of intracellular Ca 2+ in these arrhythmias is controversial. Rabbit ventricular myocytes were stimulated with a prolonged EAD-containing action potential-clamp waveform to investigate the role of Ca 2+ /calmodulin-dependent protein kinase II (CaM kinase) in I Ca,L during repolarization. I Ca,L was initially augmented, and augmentation was dependent on Ca 2+ from the sarcoplasmic reticulum because the augmentation was prevented by ryanodine or thapsigargin. I Ca,L augmentation was also dependent on CaM kinase, because it was prevented by dialysis with the inhibitor peptide AC3-I and reconstituted by exogenous constitutively active CaM kinase when Ba 2+ was substituted for bath Ca 2+ . Ultrastructural studies confirmed that endogenous CaM kinase, L-type Ca 2+ channels, and ryanodine receptors colocalized near T tubules. EAD induction was significantly reduced in current-clamped cells dialyzed with AC3-I (4/15) compared with cells dialyzed with an inactive control peptide (11/15, P = 0.013). These findings support the hypothesis that EADs are facilitated by CaM kinase." @default.
• W2218211815 created "2016-06-24" @default.
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• W2218211815 date "1999-06-01" @default.
• W2218211815 modified "2023-10-06" @default.
• W2218211815 title "CaM kinase augments cardiac L-type Ca²⁺current: a cellular mechanism for long Q-T arrhythmias" @default.
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• W2218211815 doi "https://doi.org/10.1152/ajpheart.1999.276.6.h2168" @default.
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