Apamin alters action potential profiles in post-MI rat hearts, suggesting that increased SK channel activity contributes to post-infarction electrophysiological remodeling.
Apamin effects on post-IR rat ventricular eAPs are preliminary; leaves open SK channel targeting in human cardiomyopathies.
The role of small-conductance Ca²⁺-activated K⁺-channels (SK channels) in the pathogenesis of cardiomyopathies of various etiologies remains poorly understood. The purpose of this work was to evaluate the effect of the blocker of SK channels, apamin, on the extracellularly recorded action potentials (eAPs) of subepicardial myocytes in the left ventricles of sham-operated rats and rats with myocardial infarction caused by ischemia-reperfusion. It was found that local delivery of the SK channel blocker apamin at a concentration of 500 nM to the eAP recording area did not affect the eAP profiles in the group of sham-operated rats but caused a significant slowdown in the repolarization time and a decrease in the afterhyperpolarization phase of eAPs in the group of rats with myocardial infarction. These data suggest that changes in the waveform of eAPs after infarction are associated with increased expression and/or activity of SK channels in subepicardial myocytes. The possible role of these channels in the structural and functional remodeling of the myocardium of the left ventricle of the heart after ischemia-reperfusion is discussed.
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Av et al. (2024) studied this question.
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