The opioid oxycodone use-dependently inhibits the cardiac sodium channel Na_V 1.5.

ABSTRACT:

Background and purpose

Oxycodone is a potent semi-synthetic opioid that is commonly used for the treatment of severe acute and chronic pain. However, treatment with oxycodone can lead to cardiac electrical changes, such as long QT syndrome, potentially inducing sudden cardiac arrest. Here, we investigate whether the cardiac side effects of oxycodone can be explained by modulation of the cardiac Na_v 1.5 sodium channel.

Experimental approach

Heterologously expressed human Na_v 1.5, Na_v 1.7 (HEK293 cells) or Na_v 1.8 channels (mouse N1E-115 cells) were used for whole-cell patch-clamp electrophysiology. A variety of voltage-clamp protocols were used to test the effect of oxycodone on different channel gating modalities. Human stem cell-d

SUBMITTER: Meents JE 

PROVIDER: S-EPMC6016641 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature