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The Effect of QO-58 on KCNQ1/KCNE1/IKs Potassium Channel Currents
Zhang Fan1, Li Han2, Ding Jie1, Li Yi1, Zhang Hailin1*
1Department of Pharmacology, Hebei Medical University, Shijiazhuang 050017, China; 2Department of Joint,The Third Hospitial of Hebei Medical University, Shijiazhuang 050017, China
Abstract: Slowly activated delayed rectifier potassium current (IKs) is formed by KCNQ1 and KCNE1 channel. Up regulation of KCNQ1 or KCNE1 channel currents leads to short QT syndrome. Novel compound QO-58 activates KCNQ1-5 channel. Patch clamp technique was used to study the effect of QO-58 on KCNQl/KCNEl/IKs channel currents to test the toxicity of cardiac electrophysiology. The results showed that compound QO-58 concentration-dependently activated KCNQl/KCNEl currents and shifted the KCNQl/KCNEl channel activation curve to hyperpolarization direction. QO-58 slightly enhanced IKs currents expressed in guinea pig myocytes， but had no effect on action potential duration of guinea pig papillary muscle. This suggested that the cardio toxicity of QO-58 was low. And compound QO-58 had the potential to be developed further to treat disease related with neuronal hyperexcitability.
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