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Fig. 5. Effect of mitogen-activated protein kinase (MAPK) and redox signaling pathways on carbon monoxide (CO)-induced activation of delayed rectifier K+ currents (IK) in human cardiac fibroblasts (HCFs). (A, B) Summarized current–voltage (IV) curves and (C) bar graphs of current density changes for the carbon monoxide-releasing molecule-3 (CORM3, 10 μM) effects on IK after pretreatment with SB239063 (a p38 MAPK inhibitor, 10 μM) or PD98059 (a p44/42 MAPK inhibitor, 10 μM), n = 7 (each). (D, E) Summarized I–V curves and (F) bar graphs for the effects of 10 μM CORM3 on IK after pretreatments with superoxide dismutase mimetics; MnTMPYP (50 μM) or MnTBAP (10 μM), n = 7 (each). Summarized I–V curves and bar graphs of current density changes for the effects of CORM3 on IK after (G) diphenylene iodonium (DPI, a NADPH oxidase inhibitor, 3 μM, n = 7) or (H) allopurinol (a xanthine oxidase inhibitor, 1 μM, n = 7).
Korean J Physiol Pharmacol 2022;26:25-36 https://doi.org/10.4196/kjpp.2022.26.1.25
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