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Fig. 1. Carbon monoxide (CO) increases delayed rectifier K+ currents (IK) of human cardiac fibroblasts (HCFs). Original recordings of the K+ currents were obtained by repeated voltage step depolarization from −80 to +50 mV for 400 ms duration (holding potential was –80 mV) by whole-cell mode patch clamp recordings. (A) Representative outward K+ currents show the changes before (control) and after application of (A) carbon monoxide-releasing molecule-3 (CORM3, a CO donor, 10 μM) or (B) iCORM3 (inactive CORM3, 10 μM). The currents were blocked by diphenyl phosphine oxide-1 (DPO-1, a blocker of the delayed rectifier K+ channel and the Kv1.5 channel, 1 μM). (C) Summarized current–voltage (IV) curves of steady-state currents for the effects of CORM3, iCORM3, and DPO-1. (D) Bar graphs showing the current density changes of the K+ currents at +30 mV regarding the effects of CORM3, iCORM3, and DPO-1 (n = 7, each). (E) Concentration-dependent activation curve of IK by CORM3. The solid line shows the fit based on a standard dose-response relationship, which yielded an estimated half maximal effective concentration (EC50) of 11.38 μM for CORM3. Values are mean ± SEM, *p < 0.05, **p < 0.01, and ***p < 0.001 compared to control (n = 7, each).
Korean J Physiol Pharmacol 2022;26:25-36
© Korean J Physiol Pharmacol