ArticleThe Journal of physiology2007
Window Ca2+ current and its modulation by Ca2+ release in hypertrophied cardiac myocytes from dogs with chronic atrioventricular block.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 62 citations in OpenAlex.
- A model of β-adrenergic stimulation in human ventricular cells for tissue-scale simulations of sympathetically modulated tachycardias.The Journal of physiology · 2026Article
- Arrhythmia Inducibility in the CAVB Dog Model, A Critical Analysis on Underlying Factors.Cardiovascular toxicology · 2025Article
- Article
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- PI3K/mTOR inhibitor omipalisib prolongs cardiac repolarization along with a mild proarrhythmic outcome in the AV block dog model.Frontiers in cardiovascular medicine · 2022Article
- Suppression of ventricular arrhythmias by targeting late L-type Ca2+ current.The Journal of general physiology · 2021Article
- Targeting late ICaL to close the window to ventricular arrhythmias.The Journal of general physiology · 2021Article
- Canard analysis reveals why a large Ca2+ window current promotes early afterdepolarizations in cardiac myocytes.PLoS computational biology · 2020Article
- Dynamic clamping human and rabbit atrial calcium current: narrowing IThe Journal of physiology · 2019Article
- Determinants of early afterdepolarization properties in ventricular myocyte models.PLoS computational biology · 2018Article
- Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium.Frontiers in physiology · 2018Review
- Role of sodium and calcium dysregulation in tachyarrhythmias in sudden cardiac death.Circulation research · 2015Review
- Calcium-voltage coupling in the genesis of early and delayed afterdepolarizations in cardiac myocytes.Biophysical journal · 2015Article
- Article
- The electromechanical window is no better than QT prolongation to assess risk of Torsade de Pointes in the complete atrioventricular block model in dogs.British journal of pharmacology · 2014Article
- Early afterdepolarizations in cardiac myocytes: beyond reduced repolarization reserve.Cardiovascular research · 2013Review
- Bifurcation theory and cardiac arrhythmias.American journal of cardiovascular disease · 2013Article
- Data-based theoretical identification of subcellular calcium compartments and estimation of calcium dynamics in cardiac myocytes.The Journal of physiology · 2012Article
- An updated computational model of rabbit sinoatrial action potential to investigate the mechanisms of heart rate modulation.The Journal of physiology · 2012Article
- Effects of increased preload on the force-frequency response and contractile kinetics in early stages of cardiac muscle hypertrophy.American journal of physiology. Heart and circulatory physiology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Torsades de pointes (TdP) ventricular tachycardia typically occurs in the setting of early afterdepolarizations; it contributes to arrhythmias and sudden death in congenital and acquired heart disease. Window L-type Ca2+ current (ICaL) has a central role in the arrhythmogenesis and may be particularly important under beta-adrenergic stimulation. We studied the properties of ICaL in myocytes from the dog with chronic atrioventricular block (cAVB) that has cardiac hypertrophy and an increased susceptibility to TdP. Peak ICaL densities at baseline (K+ - and Na+ -free solutions, 10 mmol l(-1) [EGTA]pip) in cAVB were comparable to control, but inactivation was shifted to the right, resulting in a larger window current area in cAVB. Under beta-adrenergic stimulation, the window current area was increased and shifted to the left, but less so in cAVB (maximum at -27 mV, versus -32 mV in control). ICaL during a step to -35 mV showed a transient reduction immediately after the peak. Test steps to 0 mV, simultaneous recording of [Ca2+]i and manipulation of sarcoplasmic reticulum (SR) Ca2+ release showed that this resulted from inhibition and fast recovery of ICaL with SR Ca2+ release. The extent of this dynamic modulation was larger in cAVB than in control (23 +/- 2% of the initially available current, versus 13 +/- 3%; P<0.05). Early afterdepolarizations (EADs) in cAVB myocytes under beta-adrenergic stimulation typically occurred in the window current voltage range and after decline of [Ca2+]i. In conclusion, in cAVB, the larger window current, its rightward shift and enhanced dynamic modulation by SR Ca2+ release may contribute to an increased incidence of EADs in cAVB under beta-adrenergic stimulation.
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