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Ilwhan Choi - One of the best experts on this subject based on the ideXlab platform.

  • blockade of voltage dependent k current in rabbit coronary arterial smooth muscle cells by the tricyclic antidepressant Clomipramine
    Journal of Pharmacological Sciences, 2018
    Co-Authors: Sung Eun Shin, Eun-taek Han, Seok-ho Hong, Amy L. Firth, Mi Seon Seo, Dae Sung Lee, Mijin Yim, Jeong Min Lee, Grace Choi, Ilwhan Choi
    Abstract:

    Abstract We investigated the effect of the tricyclic antidepressant Clomipramine on voltage-dependent K+ (Kv) channels in native rabbit coronary arterial smooth muscle cells. Our results showed that Clomipramine inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 8.61 ± 4.86 μM and a Hill coefficient (n) of 0.58 ± 0.07. The application of 10 μM Clomipramine did not affect the activation curves of the Kv channels; however, the inactivation curves of the Kv channels were shifted toward a more negative potential. The Clomipramine-induced inhibition of Kv currents was not changed by the application of train pulses (1 or 2 Hz), which demonstrated that Clomipramine inhibited Kv current in a state (use)-independent manner. Pretreatment with the Kv1.5 and Kv2.1 inhibitors, DPO-1 and guangxitoxin, respectively, partially reduced the Clomipramine-induced inhibition of Kv currents. Therefore, we concluded that Clomipramine inhibited vascular Kv channels in a concentration-dependent, but state (use)-independent manner, regardless of its own function.

Sung Eun Shin - One of the best experts on this subject based on the ideXlab platform.

  • blockade of voltage dependent k current in rabbit coronary arterial smooth muscle cells by the tricyclic antidepressant Clomipramine
    Journal of Pharmacological Sciences, 2018
    Co-Authors: Sung Eun Shin, Eun-taek Han, Seok-ho Hong, Amy L. Firth, Mi Seon Seo, Dae Sung Lee, Mijin Yim, Jeong Min Lee, Grace Choi, Ilwhan Choi
    Abstract:

    Abstract We investigated the effect of the tricyclic antidepressant Clomipramine on voltage-dependent K+ (Kv) channels in native rabbit coronary arterial smooth muscle cells. Our results showed that Clomipramine inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 8.61 ± 4.86 μM and a Hill coefficient (n) of 0.58 ± 0.07. The application of 10 μM Clomipramine did not affect the activation curves of the Kv channels; however, the inactivation curves of the Kv channels were shifted toward a more negative potential. The Clomipramine-induced inhibition of Kv currents was not changed by the application of train pulses (1 or 2 Hz), which demonstrated that Clomipramine inhibited Kv current in a state (use)-independent manner. Pretreatment with the Kv1.5 and Kv2.1 inhibitors, DPO-1 and guangxitoxin, respectively, partially reduced the Clomipramine-induced inhibition of Kv currents. Therefore, we concluded that Clomipramine inhibited vascular Kv channels in a concentration-dependent, but state (use)-independent manner, regardless of its own function.

  • Blockade of voltage-dependent K+ current in rabbit coronary arterial smooth muscle cells by the tricyclic antidepressant Clomipramine
    Elsevier, 2018
    Co-Authors: Sung Eun Shin, Eun-taek Han, Seok-ho Hong, Amy L. Firth, Mi Seon Seo, Dae Sung Lee, Mijin Yim
    Abstract:

    We investigated the effect of the tricyclic antidepressant Clomipramine on voltage-dependent K+ (Kv) channels in native rabbit coronary arterial smooth muscle cells. Our results showed that Clomipramine inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 8.61 ± 4.86 μM and a Hill coefficient (n) of 0.58 ± 0.07. The application of 10 μM Clomipramine did not affect the activation curves of the Kv channels; however, the inactivation curves of the Kv channels were shifted toward a more negative potential. The Clomipramine-induced inhibition of Kv currents was not changed by the application of train pulses (1 or 2 Hz), which demonstrated that Clomipramine inhibited Kv current in a state (use)-independent manner. Pretreatment with the Kv1.5 and Kv2.1 inhibitors, DPO-1 and guangxitoxin, respectively, partially reduced the Clomipramine-induced inhibition of Kv currents. Therefore, we concluded that Clomipramine inhibited vascular Kv channels in a concentration-dependent, but state (use)-independent manner, regardless of its own function. Keywords: Clomipramine, Voltage-dependent K+ channel, Coronary arter

Mijin Yim - One of the best experts on this subject based on the ideXlab platform.

  • blockade of voltage dependent k current in rabbit coronary arterial smooth muscle cells by the tricyclic antidepressant Clomipramine
    Journal of Pharmacological Sciences, 2018
    Co-Authors: Sung Eun Shin, Eun-taek Han, Seok-ho Hong, Amy L. Firth, Mi Seon Seo, Dae Sung Lee, Mijin Yim, Jeong Min Lee, Grace Choi, Ilwhan Choi
    Abstract:

    Abstract We investigated the effect of the tricyclic antidepressant Clomipramine on voltage-dependent K+ (Kv) channels in native rabbit coronary arterial smooth muscle cells. Our results showed that Clomipramine inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 8.61 ± 4.86 μM and a Hill coefficient (n) of 0.58 ± 0.07. The application of 10 μM Clomipramine did not affect the activation curves of the Kv channels; however, the inactivation curves of the Kv channels were shifted toward a more negative potential. The Clomipramine-induced inhibition of Kv currents was not changed by the application of train pulses (1 or 2 Hz), which demonstrated that Clomipramine inhibited Kv current in a state (use)-independent manner. Pretreatment with the Kv1.5 and Kv2.1 inhibitors, DPO-1 and guangxitoxin, respectively, partially reduced the Clomipramine-induced inhibition of Kv currents. Therefore, we concluded that Clomipramine inhibited vascular Kv channels in a concentration-dependent, but state (use)-independent manner, regardless of its own function.

  • Blockade of voltage-dependent K+ current in rabbit coronary arterial smooth muscle cells by the tricyclic antidepressant Clomipramine
    Elsevier, 2018
    Co-Authors: Sung Eun Shin, Eun-taek Han, Seok-ho Hong, Amy L. Firth, Mi Seon Seo, Dae Sung Lee, Mijin Yim
    Abstract:

    We investigated the effect of the tricyclic antidepressant Clomipramine on voltage-dependent K+ (Kv) channels in native rabbit coronary arterial smooth muscle cells. Our results showed that Clomipramine inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 8.61 ± 4.86 μM and a Hill coefficient (n) of 0.58 ± 0.07. The application of 10 μM Clomipramine did not affect the activation curves of the Kv channels; however, the inactivation curves of the Kv channels were shifted toward a more negative potential. The Clomipramine-induced inhibition of Kv currents was not changed by the application of train pulses (1 or 2 Hz), which demonstrated that Clomipramine inhibited Kv current in a state (use)-independent manner. Pretreatment with the Kv1.5 and Kv2.1 inhibitors, DPO-1 and guangxitoxin, respectively, partially reduced the Clomipramine-induced inhibition of Kv currents. Therefore, we concluded that Clomipramine inhibited vascular Kv channels in a concentration-dependent, but state (use)-independent manner, regardless of its own function. Keywords: Clomipramine, Voltage-dependent K+ channel, Coronary arter

Berend Olivier - One of the best experts on this subject based on the ideXlab platform.

  • on demand treatment of premature ejaculation with Clomipramine and paroxetine a randomized double blind fixed dose study with stopwatch assessment
    European Urology, 2004
    Co-Authors: Marcel D Waldinger, Aeilko H Zwinderman, Berend Olivier
    Abstract:

    Abstract Objective: To investigate the degree of ejaculation delay induced by on-demand treatment with 20mg paroxetine and 25mg Clomipramine and to assess the type and severity of non-sexual side-effects of treatment at the day of and the day after treatment with these drugs. Method: A randomized, double-blind, fixed-dose, on-demand study in 30 men with lifelong premature ejaculation was performed. During a 1-month baseline period and a 4-week drug treatment period patients assessed the intravaginal ejaculation latency time (IELT) at home with a stopwatch. Only men with an IELT Results: On-demand treatment with 25mg Clomipramine, with a mean DCIT of 5.14h, led to a 4.05 (95%CI: 3.26–5.02) fold-increase of the IELT. On-demand treatment with 20mg paroxetine, with a mean DCIT of 5.39h, led to a 1.41 (95%CI: 1.22–1.63) fold-increase of the IELT. Both drugs had a high incidenc of non-sexual side effects at the coitus day and the next day. At the day of coitus paroxetine led to significant sleepiness and yawning compared to Clomipramine. At the day after coitus Clomipramine induced significant nausea compared to paroxetine. Conclusion: On-demand treatment with 25mg Clomipramine led to a clinical relevant ejaculation delay. In contrast, 20mg paroxetine had no clinical relevant ejaculation delay in men with lifelong premature ejaculation with an IELT of less than 1minute. Both drugs exert mostly mild yet annoying non-sexual side effects both at the coitus day and the next day.

Mi Seon Seo - One of the best experts on this subject based on the ideXlab platform.

  • blockade of voltage dependent k current in rabbit coronary arterial smooth muscle cells by the tricyclic antidepressant Clomipramine
    Journal of Pharmacological Sciences, 2018
    Co-Authors: Sung Eun Shin, Eun-taek Han, Seok-ho Hong, Amy L. Firth, Mi Seon Seo, Dae Sung Lee, Mijin Yim, Jeong Min Lee, Grace Choi, Ilwhan Choi
    Abstract:

    Abstract We investigated the effect of the tricyclic antidepressant Clomipramine on voltage-dependent K+ (Kv) channels in native rabbit coronary arterial smooth muscle cells. Our results showed that Clomipramine inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 8.61 ± 4.86 μM and a Hill coefficient (n) of 0.58 ± 0.07. The application of 10 μM Clomipramine did not affect the activation curves of the Kv channels; however, the inactivation curves of the Kv channels were shifted toward a more negative potential. The Clomipramine-induced inhibition of Kv currents was not changed by the application of train pulses (1 or 2 Hz), which demonstrated that Clomipramine inhibited Kv current in a state (use)-independent manner. Pretreatment with the Kv1.5 and Kv2.1 inhibitors, DPO-1 and guangxitoxin, respectively, partially reduced the Clomipramine-induced inhibition of Kv currents. Therefore, we concluded that Clomipramine inhibited vascular Kv channels in a concentration-dependent, but state (use)-independent manner, regardless of its own function.

  • Blockade of voltage-dependent K+ current in rabbit coronary arterial smooth muscle cells by the tricyclic antidepressant Clomipramine
    Elsevier, 2018
    Co-Authors: Sung Eun Shin, Eun-taek Han, Seok-ho Hong, Amy L. Firth, Mi Seon Seo, Dae Sung Lee, Mijin Yim
    Abstract:

    We investigated the effect of the tricyclic antidepressant Clomipramine on voltage-dependent K+ (Kv) channels in native rabbit coronary arterial smooth muscle cells. Our results showed that Clomipramine inhibited vascular Kv channels in a concentration-dependent manner, with an IC50 value of 8.61 ± 4.86 μM and a Hill coefficient (n) of 0.58 ± 0.07. The application of 10 μM Clomipramine did not affect the activation curves of the Kv channels; however, the inactivation curves of the Kv channels were shifted toward a more negative potential. The Clomipramine-induced inhibition of Kv currents was not changed by the application of train pulses (1 or 2 Hz), which demonstrated that Clomipramine inhibited Kv current in a state (use)-independent manner. Pretreatment with the Kv1.5 and Kv2.1 inhibitors, DPO-1 and guangxitoxin, respectively, partially reduced the Clomipramine-induced inhibition of Kv currents. Therefore, we concluded that Clomipramine inhibited vascular Kv channels in a concentration-dependent, but state (use)-independent manner, regardless of its own function. Keywords: Clomipramine, Voltage-dependent K+ channel, Coronary arter