Exposure to H2O2 significantly prolonged action potential duration and increased early afterdepolarizations in wild-type murine cardiomyocytes, an effect absent in redox-dead PKA knock-in mice.
Oxidation-activated PKA type I plays a mechanistic role in ROS-induced action potential prolongation and early afterdepolarizations in murine cardiomyocytes.
Tasa de eventos absoluta: 107.6% vs 53.42%
valor p: p=0.0006
Oxidation-activated PKA type I inhibits transient outward potassium current ( I to ) and inward rectifying potassium current ( I K1 ) and contributes to ROS-induced APD prolongation as well as generation of early afterdepolarizations in murine ventricular cardiomyocytes.
Trum et al. (Fri,) conducted a other in Cardiac arrhythmias and oxidative stress. H2O2 (oxidative stress) vs. Vehicle was evaluated on Action potential duration at 90% repolarization (APD90) in WT cardiomyocytes at 2 minutes (p=0.0006). Exposure to H2O2 significantly prolonged action potential duration and increased early afterdepolarizations in wild-type murine cardiomyocytes, an effect absent in redox-dead PKA knock-in mice.
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