Sertraline potently inhibited major cardiac ion channels, including hERG, IKs, IK1, INa, and ICa, with the highest inhibitory potency for hERG channels (IC50 of 0.7 μM).
Does sertraline inhibit cardiac ion channels in HEK293 cells and rat ventricular myocytes?
Sertraline exhibits a wide spectrum of inhibitory effects on multiple cardiac ion channels, highlighting a potential mechanism for drug-induced arrhythmias and QT prolongation.
Sertraline is a commonly used antidepressant of the selective serotonin reuptake inhibitors (SSRIs) class. In these experiments, we have used the whole cell patch clamp technique to examine the effects of sertraline on the major cardiac ion channels expressed in HEK293 cells and the native voltage-gated Ca(2+) channels in rat ventricular myocytes. According to the results, sertraline is a potent blocker of cardiac K(+) channels, such as hERG, I(Ks) and I(K1). The rank order of inhibitory potency was hERG >I(K1)> I(Ks) with IC(50) values of 0.7, 10.5, and 15.2 µM, respectively. In addition to K(+) channels, sertraline also inhibited I(Na) and I(Ca), and the IC(50) values are 6.1 and 2.6 µM, respectively. Modification of these ion channels by sertraline could induce changes of the cardiac action potential duration and QT interval, and might result in cardiac arrhythmia.
Lee et al. (Sun,) reported a other. Sertraline vs. Control condition (absence of sertraline) was evaluated on Inhibition of hERG K+ channel currents (IC50). Sertraline potently inhibited major cardiac ion channels, including hERG, IKs, IK1, INa, and ICa, with the highest inhibitory potency for hERG channels (IC50 of 0.7 μM).
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