Abstract
Hydrogen sulphide (H2S), one of the most common toxic air pollutants, is an important aetiology of atrial fibrillation (AF). Pulmonary veins (PVs) and left atrium (LA) are the most important AF trigger and substrate. We investigated whether H2S may modulate the arrhythmogenesis of PVs and atria. Conventional microelectrodes and whole‐cell patch clamp were performed in rabbit PV, sinoatrial node (SAN) or atrial cardiomyocytes before and after the perfusion of NaHS with or without chelerythrine (a selective PKC inhibitor), rottlerin (a specific PKC δ inhibitor) or KB‐R7943 (a NCX inhibitor). NaHS reduced spontaneous beating rates, but increased the occurrences of delayed afterdepolarizations and burst firing in PVs and SANs. NaHS (100 μmol/L) increased IKATP and INCX in PV and LA cardiomyocytes, which were attenuated by chelerythrine (3 μmol/L). Chelerythrine, rottlerin (10 μmol/L) or KB‐R7943 (10 μmol/L) attenuated the arrhythmogenic effects of NaHS on PVs or SANs. NaHS shortened the action potential duration in LA, but not in right atrium or in the presence of chelerythrine. NaHS increased PKC activity, but did not translocate PKC isoforms α, ε to membrane in LA. In conclusion, through protein kinase C signalling, H2S increases PV and atrial arrhythmogenesis, which may contribute to air pollution‐induced AF.
Highlights
Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, increases the incidences of heart failure, stroke and mortality.[1,2,3,4] Air pollution increases the risk of AF.[5,6] Each 6.0 lg/m3 increase in PM2.5 increases the risk of AF by 26%.5 The mechanisms underlying air pollution-induced arrhythmogenesis remain unclear
We found that NaHS significantly increased the INCX and IKATP in left atrium (LA) cardiomyocytes but not in right atrium (RA) cardiomyocytes, which may result in the shortening of action potential duration (APD) in NaHStreated LA
Hydrogen sulphide increases the arrhythmogenesis of Pulmonary veins (PVs) and sinoatrial node (SAN) and differentially regulates the cardiac electrophysiology of the LA and RA
Summary
Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, increases the incidences of heart failure, stroke and mortality.[1,2,3,4] Air pollution increases the risk of AF.[5,6] Each 6.0 lg/m3 increase in PM2.5 increases the risk of AF by 26%.5 The mechanisms underlying air pollution-induced arrhythmogenesis remain unclear. Air pollution is associated with autonomic tone changes,[7] inflammation[8] and cardiac ischaemia.[9] Hydrogen sulphide (H2S) is one of the most common toxic air pollutants.[10] H2S is produced by the anaerobic. H2S plays a critical role in cell signalling[25] and attenuates ischaemia-reperfusion injury by activating the ATP-sensitive potassium channel (KATP).[26] The activation of the KATP channel shortens the action potential duration (APD), which may increase the risk of AF by facilitating the genesis of re-entry circuits. H2S may modulate the electrical activity of PVs, atria and SANs and increase the risk of air pollution-induced AF. This study explored the effects of H2S on PVs, atria and SANs, and investigated the potential underlying mechanisms
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