June 12, 2009British Journal of PharmacologyOpen Access

Probing the mechanisms underlying modulation of quinidine sensitivity to cardiac IKsblock by protein kinase A‐mediated IKsphosphorylation

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Population

Cardiac I(Ks) channels (wild-type and KCNQ1 mutants with three PKA site residues mutated to aspartic acid)

Comparison

Quinidine with PKA stimulation and… vs Quinidine without PKA stimulation or without…

Design

Preclinical

Authors

TYTao YangTang Du Hospital HKHideaki KankiOsaka City University WZWei ZhangUniversity of Akron

Discussion

Member takes

Implication

PKA may blunt quinidine block of IKs channels; hypothesis-generating for reduced proarrhythmic risk, needs in vivo confirmation.

Structured PICO

Population

Cardiac I(Ks) channels (wild-type and KCNQ1 mutants with three PKA site residues mutated to aspartic acid)

Intervention

Quinidine (100 microM) with PKA stimulation and hyperpolarizing prepulses to -120 mV

Comparator

Quinidine without PKA stimulation or without hyperpolarizing prepulses

Outcome

Extent of quinidine block of activating current at +60 mVsurrogate

PKA-induced phosphorylation blunts quinidine block of cardiac I(Ks) channels by destabilizing the drug-channel interaction, potentially protecting against drug-induced pro-arrhythmias.

Cite This Study

Yang et al. (2009) studied this question.

synapsesocial.com/papers/6a71fee678a11c550e0be70b https://doi.org/10.1111/j.1476-5381.2009.00293.x

View Full Paper

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Probing the mechanisms underlying modulation of quinidine sensitivity to cardiac IKsblock by protein kinase A‐mediated IKsphosphorylation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Probing the mechanisms underlying modulation of quinidine sensitivity to cardiac IKsblock by protein kinase A‐mediated IKsphosphorylation

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider