Key result
Intracellular calcium reduction or CaMKII inhibition decreases late sodium current amplitude in ventricular myocytes.
Why the study?
Enhancement of the late sodium current increases cardiac arrhythmia propensity whereas its suppression is antiarrhythmic, prompting investigation of this current under action potential voltage-clamp conditions.
Does intracellular calcium reduction or CaMKII inhibition reduce the late sodium current in canine ventricular myocytes?
Population
Canine ventricular cardiomyocytes
Comparison
Inhibition with GS967 and tetrodotoxin under reduced intracellular Ca2+ or CaMKII inhibition vs control conditions
Design
Action potential voltage-clamp experimental study
Authors
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Hypothesis-generating for CaMKII regulation of late sodium current; leaves open translation to human arrhythmias or therapy.
Does intracellular calcium reduction or CaMKII inhibition reduce the late sodium current in canine ventricular myocytes?
This study demonstrates that the late sodium current is physiologically regulated by intracellular calcium via CaMKII in canine ventricular myocytes, providing mechanistic insights into arrhythmogenesis.
Kiss et al. (2021) studied Healthy. Intracellular calcium reduction and CaMKII inhibition vs. Control conditions was evaluated on Amplitude and integral of the late sodium current (INaL). Reduction of intracellular calcium or inhibition of CaMKII significantly decreased the amplitude and integral of the late sodium current in canine ventricular myocytes.
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