Abstract
Introduction: Pulmonary veins (PVs) are known to initiate paroxysmal atrial fibrillation. T-type calcium current (ICa-T) has a role in normal and abnormal automaticity of cardiomyocytes. The aim of this study was to evaluate whether ICa-T contributes to PV electrical activity. Methods and Results: By whole-cell clamp techniques in rabbit myocytes, I Ca-T was identified in 12 (39%) of 31 PV cardiomyocytes with pacemaker activity, 2 (9%) of 23 PV cardiomyocytes without pacemaker activity, and 2 (15%) of 13 atrial myocytes (P < 0.05). Maximum ICa-L and ICa-T densities from PV cardiomyocytes with pacemaker activity were 6.87 ± 2.17 pA/pF and 1.38 ± 0.69 pA/pF, respectively. Nickel (40 μM) decreased the spontaneous activity in 5 (36%) of 14 PV cardiomyocytes (3.1 ± 0.6 Hz vs 2.2 ± 0.5 Hz, P < 0.05), reduced the amplitudes of delayed afterdepolarization from 13 ± 1 mV to 7 ± 1 mV (n = 4, P < 0.05) and inhibited transient inward currents from 1.2 ± 0.2 pA/pF to 0.7 ± 0.1 pA/pF (n = 11, P < 0.01). Conclusions: We conclude that ICa-T contributes to PV pacemaker activity and triggered activity, which are of functional importance in PV arrhythmogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 567-571 |
| Number of pages | 5 |
| Journal | Journal of Cardiovascular Electrophysiology |
| Volume | 15 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 2004 |
Keywords
- Calcium channel
- Nickel
- Pulmonary vein
- Transient inward current
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)
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