Escitalopram, a selective serotonin reuptake inhibitor, inhibits voltage-dependent K+ channels in coronary arterial smooth muscle cells
Han Sol Kim1,#, Hongliang Li1,#, Hye Won Kim1, Sung Eun Shin1, Mi Seon Seo1, Jin Ryeol An1, Kwon-Soo Ha2, Eun-Taek Han3, Seok-Ho Hong4, Il-Whan Choi5, Grace Choi6, Dae-sung Lee6, and Won Sun Park1,*
Departments of 1Physiology, 2Molecular and Cellular Biochemistry, 3Medical Environmental Biology and Tropical Medicine, 4Internal Medicine, Kangwon National University School of Medicine, Chuncheon 24341, 5Department of Microbiology, Inje University College of Medicine, Busan 47392, 6Department of Applied Research, National Marine Biodiversity Institute of Korea, Seocheon 33662, Korea
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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 IC50 value and Hill coefficient for escitalopram-induced inhibition of Kv channels were 9.54±1.33 µM and 0.75±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.