Inhibition of cardiac HERG potassium channels by antidepressant maprotiline
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Many drugs block delayed rectifier K channels and prolong the cardiac action potential duration. Here we investigate the molecular mechanisms of voltage-dependent block of human ether-a-go-go-related gene (HERG) K channels expressed in cells HEK-293 and Xenopus oocytes by maprotiline. The IC50 determined at 0 mV on HERG expressed HEK-293 cell and oocytes was 5.2 and 23.7 μM, respectively. Block of HERG expressed in oocytes by maprotiline was enhanced by progressive membrane depolarization and accompanied by a negative shift in the voltage dependence of channel activation. The potency of maprotiline was reduced 7-fold by point mutation of a key aromatic residue (F656T) and 3-fold for Y652A, both located in the S6 domain. The mutation Y652A inverted the voltage dependence of HERG channel block by maprotiline. Together, these results suggest that voltage-dependent block of HERG results from gating dependent changes in the accessibility of Y652, a critical component of the drug binding site. © 2005 Elsevier B.V. All rights reserved.
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Many drugs block delayed rectifier K%2b channels and prolong the cardiac action potential duration. Here we investigate the molecular mechanisms of voltage-dependent block of human ether-a-go-go-related gene (HERG) K %2b channels expressed in cells HEK-293 and Xenopus oocytes by maprotiline. The IC50 determined at 0 mV on HERG expressed HEK-293 cell and oocytes was 5.2 and 23.7 μM, respectively. Block of HERG expressed in oocytes by maprotiline was enhanced by progressive membrane depolarization and accompanied by a negative shift in the voltage dependence of channel activation. The potency of maprotiline was reduced 7-fold by point mutation of a key aromatic residue (F656T) and 3-fold for Y652A, both located in the S6 domain. The mutation Y652A inverted the voltage dependence of HERG channel block by maprotiline. Together, these results suggest that voltage-dependent block of HERG results from gating dependent changes in the accessibility of Y652, a critical component of the drug binding site. © 2005 Elsevier B.V. All rights reserved.
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Acquired long QT syndrome; Arrhythmia; HERG potassium channel; IKr; Maprotiline; QT interval; Rapid delayed rectifier; Torsade de pointes antidepressant agent; maprotiline; potassium channel HERG; animal cell; article; cell membrane depolarization; cell strain HEK293; controlled study; drug binding site; drug effect; drug mechanism; drug potency; female; gene expression; human; human cell; IC 50; molecular mechanics; nonhuman; oocyte; point mutation; priority journal; Xenopus; Animals; Antidepressive Agents, Second-Generation; Binding Sites; Dose-Response Relationship, Drug; Electric Stimulation; Ether-A-Go-Go Potassium Channels; Female; Gene Expression; Humans; Maprotiline; Membrane Potentials; Oocytes; Point Mutation; Xenopus
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