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Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis
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| Zeitschriftentitel: | American Journal of Physiology-Heart and Circulatory Physiology |
|---|---|
| Personen und Körperschaften: | , , , |
| In: | American Journal of Physiology-Heart and Circulatory Physiology, 289, 2005, 4, S. H1584-H1593 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Balasubramaniam, Richard Chawla, Sangeeta Grace, Andrew A. Huang, Christopher L.-H. Balasubramaniam, Richard Chawla, Sangeeta Grace, Andrew A. Huang, Christopher L.-H. |
|---|---|
| author |
Balasubramaniam, Richard Chawla, Sangeeta Grace, Andrew A. Huang, Christopher L.-H. |
| spellingShingle |
Balasubramaniam, Richard Chawla, Sangeeta Grace, Andrew A. Huang, Christopher L.-H. American Journal of Physiology-Heart and Circulatory Physiology Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
| author_sort |
balasubramaniam, richard |
| spelling |
Balasubramaniam, Richard Chawla, Sangeeta Grace, Andrew A. Huang, Christopher L.-H. 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.01250.2004 <jats:p> Heart failure leading to ventricular arrhythmogenesis is a major cause of clinical mortality and has been associated with a leak of sarcoplasmic reticular Ca<jats:sup>2+</jats:sup> into the cytosol due to increased open probabilities in cardiac ryanodine receptor Ca<jats:sup>2+</jats:sup>-release channels. Caffeine similarly increases such open probabilities, and so we explored its arrhythmogenic effects on intact murine hearts. A clinically established programmed electrical stimulation protocol adapted for studies of isolated intact mouse hearts demonstrated that caffeine (1 mM) increased the frequency of ventricular tachycardia from 0 to 100% yet left electrogram duration and latency unchanged during programmed electrical stimulation, thereby excluding slowed conduction as a cause of arrhythmogenesis. We then used fluorescence measurements of intracellular Ca<jats:sup>2+</jats:sup> concentration in isolated mouse ventricular cells to investigate parallel changes in Ca<jats:sup>2+</jats:sup> homeostasis associated with these arrhythmias. Both caffeine (1 mM) and FK506 (30 μM) reduced electrically evoked cytosolic Ca<jats:sup>2+</jats:sup> transients yet increased the frequency of spontaneous Ca<jats:sup>2+</jats:sup>-release events. Diltiazem (1 μM) but not nifedipine (1 μM) pretreatment suppressed these increases in frequency. Identical concentrations of diltiazem but not nifedipine correspondingly suppressed the arrhythmogenic effects of caffeine in whole hearts. These findings thus directly implicate spontaneous Ca<jats:sup>2+</jats:sup> waves in triggered arrhythmogenesis in intact hearts. </jats:p> Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca<sup>2+</sup> homeostasis American Journal of Physiology-Heart and Circulatory Physiology |
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American Journal of Physiology-Heart and Circulatory Physiology |
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| title |
Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_unstemmed |
Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_full |
Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_fullStr |
Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_full_unstemmed |
Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_short |
Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_sort |
caffeine-induced arrhythmias in murine hearts parallel changes in cellular ca<sup>2+</sup> homeostasis |
| topic |
Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
| url |
http://dx.doi.org/10.1152/ajpheart.01250.2004 |
| publishDate |
2005 |
| physical |
H1584-H1593 |
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<jats:p> Heart failure leading to ventricular arrhythmogenesis is a major cause of clinical mortality and has been associated with a leak of sarcoplasmic reticular Ca<jats:sup>2+</jats:sup> into the cytosol due to increased open probabilities in cardiac ryanodine receptor Ca<jats:sup>2+</jats:sup>-release channels. Caffeine similarly increases such open probabilities, and so we explored its arrhythmogenic effects on intact murine hearts. A clinically established programmed electrical stimulation protocol adapted for studies of isolated intact mouse hearts demonstrated that caffeine (1 mM) increased the frequency of ventricular tachycardia from 0 to 100% yet left electrogram duration and latency unchanged during programmed electrical stimulation, thereby excluding slowed conduction as a cause of arrhythmogenesis. We then used fluorescence measurements of intracellular Ca<jats:sup>2+</jats:sup> concentration in isolated mouse ventricular cells to investigate parallel changes in Ca<jats:sup>2+</jats:sup> homeostasis associated with these arrhythmias. Both caffeine (1 mM) and FK506 (30 μM) reduced electrically evoked cytosolic Ca<jats:sup>2+</jats:sup> transients yet increased the frequency of spontaneous Ca<jats:sup>2+</jats:sup>-release events. Diltiazem (1 μM) but not nifedipine (1 μM) pretreatment suppressed these increases in frequency. Identical concentrations of diltiazem but not nifedipine correspondingly suppressed the arrhythmogenic effects of caffeine in whole hearts. These findings thus directly implicate spontaneous Ca<jats:sup>2+</jats:sup> waves in triggered arrhythmogenesis in intact hearts. </jats:p> |
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| author | Balasubramaniam, Richard, Chawla, Sangeeta, Grace, Andrew A., Huang, Christopher L.-H. |
| author_facet | Balasubramaniam, Richard, Chawla, Sangeeta, Grace, Andrew A., Huang, Christopher L.-H., Balasubramaniam, Richard, Chawla, Sangeeta, Grace, Andrew A., Huang, Christopher L.-H. |
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| description | <jats:p> Heart failure leading to ventricular arrhythmogenesis is a major cause of clinical mortality and has been associated with a leak of sarcoplasmic reticular Ca<jats:sup>2+</jats:sup> into the cytosol due to increased open probabilities in cardiac ryanodine receptor Ca<jats:sup>2+</jats:sup>-release channels. Caffeine similarly increases such open probabilities, and so we explored its arrhythmogenic effects on intact murine hearts. A clinically established programmed electrical stimulation protocol adapted for studies of isolated intact mouse hearts demonstrated that caffeine (1 mM) increased the frequency of ventricular tachycardia from 0 to 100% yet left electrogram duration and latency unchanged during programmed electrical stimulation, thereby excluding slowed conduction as a cause of arrhythmogenesis. We then used fluorescence measurements of intracellular Ca<jats:sup>2+</jats:sup> concentration in isolated mouse ventricular cells to investigate parallel changes in Ca<jats:sup>2+</jats:sup> homeostasis associated with these arrhythmias. Both caffeine (1 mM) and FK506 (30 μM) reduced electrically evoked cytosolic Ca<jats:sup>2+</jats:sup> transients yet increased the frequency of spontaneous Ca<jats:sup>2+</jats:sup>-release events. Diltiazem (1 μM) but not nifedipine (1 μM) pretreatment suppressed these increases in frequency. Identical concentrations of diltiazem but not nifedipine correspondingly suppressed the arrhythmogenic effects of caffeine in whole hearts. These findings thus directly implicate spontaneous Ca<jats:sup>2+</jats:sup> waves in triggered arrhythmogenesis in intact hearts. </jats:p> |
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| spelling | Balasubramaniam, Richard Chawla, Sangeeta Grace, Andrew A. Huang, Christopher L.-H. 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.01250.2004 <jats:p> Heart failure leading to ventricular arrhythmogenesis is a major cause of clinical mortality and has been associated with a leak of sarcoplasmic reticular Ca<jats:sup>2+</jats:sup> into the cytosol due to increased open probabilities in cardiac ryanodine receptor Ca<jats:sup>2+</jats:sup>-release channels. Caffeine similarly increases such open probabilities, and so we explored its arrhythmogenic effects on intact murine hearts. A clinically established programmed electrical stimulation protocol adapted for studies of isolated intact mouse hearts demonstrated that caffeine (1 mM) increased the frequency of ventricular tachycardia from 0 to 100% yet left electrogram duration and latency unchanged during programmed electrical stimulation, thereby excluding slowed conduction as a cause of arrhythmogenesis. We then used fluorescence measurements of intracellular Ca<jats:sup>2+</jats:sup> concentration in isolated mouse ventricular cells to investigate parallel changes in Ca<jats:sup>2+</jats:sup> homeostasis associated with these arrhythmias. Both caffeine (1 mM) and FK506 (30 μM) reduced electrically evoked cytosolic Ca<jats:sup>2+</jats:sup> transients yet increased the frequency of spontaneous Ca<jats:sup>2+</jats:sup>-release events. Diltiazem (1 μM) but not nifedipine (1 μM) pretreatment suppressed these increases in frequency. Identical concentrations of diltiazem but not nifedipine correspondingly suppressed the arrhythmogenic effects of caffeine in whole hearts. These findings thus directly implicate spontaneous Ca<jats:sup>2+</jats:sup> waves in triggered arrhythmogenesis in intact hearts. </jats:p> Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca<sup>2+</sup> homeostasis American Journal of Physiology-Heart and Circulatory Physiology |
| spellingShingle | Balasubramaniam, Richard, Chawla, Sangeeta, Grace, Andrew A., Huang, Christopher L.-H., American Journal of Physiology-Heart and Circulatory Physiology, Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis, Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
| title | Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_full | Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_fullStr | Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_full_unstemmed | Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_short | Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| title_sort | caffeine-induced arrhythmias in murine hearts parallel changes in cellular ca<sup>2+</sup> homeostasis |
| title_unstemmed | Caffeine-induced arrhythmias in murine hearts parallel changes in cellular Ca2+ homeostasis |
| topic | Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
| url | http://dx.doi.org/10.1152/ajpheart.01250.2004 |