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Escitalopram, a selective serotonin reuptake inhibitor, inhibits voltage-dependent K+ channels in coronary arterial smooth muscle cells

  • Kim, Han Sol (Department of Physiology, Kangwon National University School of Medicine) ;
  • Li, Hongliang (Department of Physiology, Kangwon National University School of Medicine) ;
  • Kim, Hye Won (Department of Physiology, Kangwon National University School of Medicine) ;
  • Shin, Sung Eun (Department of Physiology, Kangwon National University School of Medicine) ;
  • Seo, Mi Seon (Department of Physiology, Kangwon National University School of Medicine) ;
  • An, Jin Ryeol (Department of Physiology, Kangwon National University School of Medicine) ;
  • Ha, Kwon-Soo (Department of Molecular and Cellular Biochemistry, Kangwon National University School of Medicine) ;
  • Han, Eun-Taek (Department of Medical Environmental Biology and Tropical Medicine, Kangwon National University School of Medicine) ;
  • Hong, Seok-Ho (Department of Internal Medicine, Kangwon National University School of Medicine) ;
  • Choi, Il-Whan (Department of Microbiology, Inje University College of Medicine) ;
  • Choi, Grace (Department of Applied Research, National Marine Biodiversity Institute of Korea) ;
  • Lee, Dae-sung (Department of Applied Research, National Marine Biodiversity Institute of Korea) ;
  • Park, Won Sun (Department of Physiology, Kangwon National University School of Medicine)
  • Received : 2017.02.08
  • Accepted : 2017.03.08
  • Published : 2017.07.01

Abstract

We investigated the inhibitory effect of escitalopram, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent $K^+$ (Kv) channels in freshly separated from rabbit coronary arterial smooth muscle cells. The application of escitalopram rapidly inhibited vascular Kv channels. Kv currents were progressively inhibited by an increase in the concentrations of escitalopram, suggesting that escitalopram inhibited vascular Kv currents in a concentration-dependent manner. The $IC_{50}$ value and Hill coefficient for escitalopram-induced inhibition of Kv channels were $9.54{\pm}1.33{\mu}M$ and $0.75{\pm}0.10$, respectively. Addition of escitalopram did not alter the steady-state activation and inactivation curves, suggesting that the voltage sensors of the channels were not affected. Pretreatment with inhibitors of Kv1.5 and/or Kv2.1 did not affect the inhibitory action of escitalopram on vascular Kv channels. From these results, we concluded that escitalopram decreased the vascular Kv current in a concentration-dependent manner, independent of serotonin reuptake inhibition.

Keywords

References

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