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December 22, 2011AJP Cell Physiology

Calmodulin kinase II and protein kinase C mediate the effect of increased intracellular calcium to augment late sodium current in rabbit ventricular myocytes

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Why the study?

Does inhibition of CaMKII and PKC reduce calcium-induced augmentation of late sodium current in rabbit ventricular myocytes?

Population

Rabbit ventricular myocytes

Comparison

Dialysis with solutions containing various… vs Baseline or lower concentrations of [Ca], or…

Design

Preclinical

Authors

JMJihua MaALAntao LuoLWLin Wu

Discussion

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Overview

Inhibiting CaMKII/PKC reverses calcium-augmented late sodium current in myocytes; hypothesis-generating for arrhythmia targets.

Structured PICO

Does inhibition of CaMKII and PKC reduce calcium-induced augmentation of late sodium current in rabbit ventricular myocytes?

P
Population
Rabbit ventricular myocytes
I
Intervention
Dialysis with solutions containing various concentrations of intracellular calcium ([Ca(2+)](i)) from 0.1 to 1.0 μM, with or without CaMKII inhibitors (KN-93, autocamtide-2-related inhibitory peptide II) and PKC inhibitors (bisindolylmaleimide, Gö-6976) or activators (Phorbol myristoyl acetate)
C
Comparator
Baseline or lower concentrations of [Ca(2+)](i) (e.g., 0.1 μM), or absence of kinase inhibitors
O
Outcome
Late sodium current (I(Na.L)) amplitude, mean Na(+) channel open probability, and channel mean open-timesurrogate

Both CaMKII and PKC mediate the calcium-induced augmentation of late sodium current in ventricular myocytes, suggesting their inhibition could be a therapeutic target for calcium overload-induced arrhythmias.

Cite This Study

Ma et al. (2011) studied this question.

synapsesocial.com/papers/6a8c4bcdefbb049866866f69https://doi.org/10.1152/ajpcell.00374.2011
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