Key result
Carvedilol prevents spontaneous arrhythmogenic Ca2+ waves and inhibits sodium and calcium currents by acting directly on the SR ryanodine receptor Ca2+ release channel in adult atrial myocytes.
Why the study?
Does carvedilol prevent arrhythmogenic Ca2+ waves in adult atrial myocytes?
Does carvedilol prevent arrhythmogenic Ca2+ waves in adult atrial myocytes?
Answers are grounded in this paper and cite their sources.
Carvedilol exerts direct antiarrhythmic effects in adult atrial myocytes by acting on the SR ryanodine receptor Ca2+ release channel to prevent arrhythmogenic Ca2+ waves, though it also inhibits sodium and calcium currents leading to ECC failure.
Here we show that the clinically widely used β-blocker carvedilol has profound effects on Ca 2+ signaling and ion currents, but also antiarrhythmic effects in adult atrial myocytes. Carvedilol inhibits sodium and calcium currents and leads to failure of ECC but also prevents spontaneous Ca 2+ release from cellular sarcoplasmic reticulum (SR) Ca 2+ stores in form of arrhythmogenic Ca 2+ waves. The antiarrhythmic effect occurs by carvedilol acting directly on the SR ryanodine receptor Ca 2+ release channel.
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Martínez‐Hernández et al. (2020) studied Arrhythmogenicity in adult atrial myocytes. Carvedilol was evaluated on Ca2+ signaling, ion currents, and arrhythmogenic Ca2+ waves. Carvedilol prevents spontaneous arrhythmogenic Ca2+ waves and inhibits sodium and calcium currents by acting directly on the SR ryanodine receptor Ca2+ release channel in adult atrial myocytes.
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