Blockade of K⁺ and Ca²⁺ Channels by Azole Antifungal Agents in Neonatal Rat Ventricular Myocytes

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  • Sung Dong-Jun
    Department of Physiology, Institute of Functional Genomics, & Research Institute of Medical Science, School of Medicine, Konkuk University
  • Kim Jae-Gon
    Department of Physiology, Institute of Functional Genomics, & Research Institute of Medical Science, School of Medicine, Konkuk University
  • Won Kyung Jong
    Department of Physiology, Institute of Functional Genomics, & Research Institute of Medical Science, School of Medicine, Konkuk University
  • Kim Bokyung
    Department of Physiology, Institute of Functional Genomics, & Research Institute of Medical Science, School of Medicine, Konkuk University
  • Shin Ho Chul
    Department of Veterinary Pharmacology and Toxicology, College of Veterinary Medicine, Konkuk University
  • Park Jae-Yong
    Department of Physiology, Institute of Health Science, and Medical Research Center for Neural Dysfunction, School of Medicine, Gyeongsang National University
  • Bae Young Min
    Department of Physiology, Institute of Functional Genomics, & Research Institute of Medical Science, School of Medicine, Konkuk University

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タイトル別名
  • Blockade of K<sup>+</sup> and Ca<sup>2+</sup> Channels by Azole Antifungal Agents in Neonatal Rat Ventricular Myocytes

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Some azole antifungal agents induce long QT syndrome and arrhythmias. Although composite functions of ion channels in cardiomyocytes contribute to the shaping of action potentials, information on the effects of azole antifungal agents on ion currents, except human-ether-a-go-go-related gene (HERG) K+ currents, is largely lacking. Using the whole cell patch-clamp technique, we investigated the effects of four azole agents (miconazole, ketoconazole, fluconazole, and itraconazole) on inward rectifying K+ currents (IKir), voltage-gated L-type Ca2+ currents (ICaL), and delayed rectifier K+ currents (IKdr) in rat neonate ventricular myocytes. Strikingly, miconazole and ketoconazole strongly inhibited IKir, IKdr, and ICaL at clinically relevant concentrations. The IC50 values of miconazole for IKdr, IKir, and ICaL inhibition were 2.5, 10.4, and 3.0 µM, respectively. The IC50 values of ketoconazole for IKdr, IKir and ICaL inhibition were 3.2, 20.8, and 3.5 µM, respectively. Fluconazole and itraconazole had relatively little effect on ion currents. These findings indicate that miconazole and ketoconazole are multiple ion channel inhibitors in cardiomyocytes. We suggest that it is necessary to consider this inhibition of ion channels by azole agents when assessing cardiovascular side effects.

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