Key Points
- To determine how the ryanodine receptor stabilizer K201 alters electrical firing, ionic currents, and calcium regulation in pulmonary vein cardiomyocytes.
- Isolated single cardiomyocytes from rabbit pulmonary veins.
- Measured ionic currents, action potentials, and intracellular calcium before and after application of K201 (0.1, 0.3, and 1 µM) using whole-cell patch-clamp and indo-1 fluorimetry.
- K201 (0.1–1 µM) concentration-dependently reduced spontaneous firing rates, decreased the amplitude of delayed afterdepolarizations, and prolonged action potential duration.
- K201 suppressed L-type calcium currents, Na+/Ca2+ exchanger currents, transient inward currents, and calcium transients, with 1 µM also decreasing sarcoplasmic reticulum calcium content.
- Both pretreatment and acute administration of 0.3 µM K201 significantly attenuated arrhythmogenic activity triggered by 10 nM isoprenaline.
Structured PICO
Does K201 reduce arrhythmogenic activity in isolated rabbit pulmonary vein cardiomyocytes?
PPopulationIsolated single cardiomyocytes from rabbit pulmonary vein
IInterventionK201 (0.1, 0.3, 1 microM)
CComparatorBaseline (before administration of K201)
OOutcomeArrhythmogenic activity and calcium regulation (ionic currents and intracellular calcium)surrogate
K201 reduces arrhythmogenic activity and attenuates isoprenaline-induced arrhythmogenicity in rabbit pulmonary vein cardiomyocytes, highlighting its potential as an anti-arrhythmic agent.