June 22, 2012Circulation Research
Functional Na V 1.8 Channels in Intracardiac Neurons
Key result
The NaV1.8 blocker A-803467 significantly reduced sodium current density and action potential firing frequency in murine intracardiac neurons, but had no effect in isolated ventricular myocytes.
Population
Mouse heart tissue (intracardiac neurons and isolated ventricular myocytes)
Design
Preclinical
Authors
Discussion
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Member takes
Implication
May support selective NaV1.8 targeting in cardiac neurons; leaves open translation to human arrhythmia therapy.
Structured PICO
P
Population
Mouse heart tissue (intracardiac neurons and isolated ventricular myocytes)
I
Intervention
NaV1.8 blocker A-803467 (0.5-2 μmol/L)
O
Outcome
Sodium current (INa) density, gating kinetics, and action potential firing frequencysurrogate
The study demonstrates the functional presence of NaV1.8 channels in intracardiac neurons, suggesting a novel role in regulating cardiac electrical activity.
Cite This Study
Verkerk et al. (2012) studied this question. A-803467 was evaluated on Sodium current (INa) density and action potential firing frequency. The NaV1.8 blocker A-803467 significantly reduced sodium current density and action potential firing frequency in murine intracardiac neurons, but had no effect in isolated ventricular myocytes.