Key result
SK channel activator NS309 shortens ventricular action potentials, an effect blocked by apamin.
Why the study?
Does pharmacological modulation of SK channels alter the profiles of extracellularly recorded action potentials in ventricular myocytes of intact rats?
Does pharmacological modulation of SK channels alter the profiles of extracellularly recorded action potentials in ventricular myocytes of intact rats?
SK channel activation shortens ventricular action potentials in rat hearts, suggesting functional SK channels are present in ventricles and may serve as a potential target for treating impaired cardiomyocyte repolarization.
Hypothesis-generating for SK channel effects on rat ventricular APs; leaves open clinical relevance in human ventricular arrhythmias.
Some cardiac disorders can manifest as alterations in the shape of action potentials (APs), which is a risk factor for the development of cardiovascular diseases. Small-conductance Ca2+-activated potassium channels (SK channels) play an important role in the regulation of cardiac muscle excitation. However, their (patho)physiological role in the ventricles, unlike in the atria, remains insufficiently studied. We tested the hypothesis that in ventricular myocytes of intact rats, pharmacological modulation of SK channels can play a decisive role in shaping the profiles of extracellularly recorded APs (eAPs). The SK channel blocker apamin had a negligible effect on eAP repolarization. However, the SK channel activator NS309 led to a significant shortening of eAPs. Apamin, when co-applied with NS309, prevented the effect of NS309 on the eAP profile. The data obtained indicate that functional SK channels are initially present both in the T-system and in the surface membrane of ventricular myocytes of rat hearts. This suggests that SK channel activation may be considered a potential method for the prevention and treatment of cardiac diseases associated with impaired cardiomyocyte repolarization.
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Kubasov et al. (2026) studied this question. NS309 and apamin vs. Baseline / apamin alone was evaluated on Profiles of extracellularly recorded action potentials (eAPs). The SK channel activator NS309 significantly shortened extracellular action potentials in isolated rat ventricular myocytes, an effect that was prevented by the blocker apamin.
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