Key result
Late INa inhibitors suppressed the diastolic depolarization and automaticity of guinea pig pulmonary vein myocardium without affecting the contractile force of the working myocardium.
Why the study?
The role of the Na+ current in the automaticity of the pulmonary vein myocardium remained to be examined.
Does modulation of the persistent Na+ current affect diastolic depolarization and automaticity in guinea pig pulmonary vein myocardium?
Does modulation of the persistent Na+ current affect diastolic depolarization and automaticity in guinea pig pulmonary vein myocardium?
Late INa is involved in the diastolic depolarization and automaticity of the pulmonary vein myocardium, suggesting late INa inhibitors could be effective for atrial fibrillation with minimal adverse effects on working myocardium contractility.
Should not yet change AF practice; leaves open human translation of late INa effects on pulmonary-vein automaticity.
The role of the Na + current in the automaticity of the pulmonary vein myocardium was examined in isolated guinea pig pulmonary vein cardiomyocytes and tissue preparations. Tetrodotoxin inhibited the automaticity of pulmonary vein tissue preparations by suppressing the diastolic depolarization of the action potential. ATX-II, which increased the density of persistent component of the Na + current (late I Na ), induced a depolarization of the resting membrane potential followed by spontaneous firing of action potentials. GS-458967, which inhibited the late I Na , suppressed the diastolic depolarization and the firing of action potentials. Pilsicainide, which inhibited only the transient component of Na + current (peak I Na ), had no effect on the firing frequency. GS-458967 had no effect on the contractile force of the working myocardium. In conclusion, late I Na is involved in the diastolic depolarization and automaticity of the pulmonary vein myocardium. Late I Na inhibitors appear to be effective therapeutic agents for atrial fibrillation with minimum adverse effects on the working myocardium.
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Irie et al. (2019) studied Atrial fibrillation (experimental model). Late INa inhibitors (GS-458967, Tetrodotoxin) was evaluated on Diastolic depolarization and automaticity of the pulmonary vein myocardium. Late INa inhibitors suppressed the diastolic depolarization and automaticity of guinea pig pulmonary vein myocardium without affecting the contractile force of the working myocardium.
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