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March 1, 1996Circulation Research

Class III Antiarrhythmic Drugs Block HERG, a Human Cardiac Delayed Rectifier K+Channel

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Population

Xenopus oocytes expressing HERG channels

Design

Preclinical

Authors

PSPeter SpectorElectrophysiologyMCMark CurranWorcester Polytechnic InstituteMKMark T. KeatingElectrophysiology

Discussion

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Implication

Cautions against direct human translation; supports HERG as molecular basis of IKr in preclinical models.

Structured PICO

P
Population
Xenopus oocytes expressing HERG channels
I
Intervention
Class III antiarrhythmic drugs (E-4031 and MK-499)
O
Outcome
Blockade of HERG current measured by two-microelectrode voltage-clamp techniquessurrogate

Class III antiarrhythmic drugs like MK-499 preferentially block open HERG channels, providing mechanistic evidence that HERG subunits form the cardiac delayed rectifier K+ current I(Kr).

Cite This Study

Spector et al. (1996) studied this question.

synapsesocial.com/papers/6a74db836a5eb4b8f509306ehttps://doi.org/10.1161/01.res.78.3.499
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents.1990 · 1,472 citations
  2. 2Cellular electrophysiology of WAY-123,398, a new class III antiarrhythmic agent: specificity of IK block and lack of reverse use dependence in cat ventricular myocytes1993 · 54 citations
  3. 3Use-dependent block and use-dependent unblock of the delayed rectifier K+ current by almokalant in rabbit ventricular myocytes.1993 · 137 citations
  4. 4Conductance and kinetics of delayed rectifier potassium channels in nodal cells of the rabbit heart.1987 · 338 citations
  5. 5K+ currents and K+ channel mRNA in cultured atrial cardiac myocytes (AT-1 cells).1994 · 76 citations