Targeting the L-type Ca(2+) channel is a suitable strategy for developing drugs to modify channel function during hypoxia or oxidative stress to prevent induction of arrhythmia.
Can drugs targeting the L-type Ca(2+) channel modify channel function during hypoxia or oxidative stress to prevent induction of arrhythmia?
The L-type calcium channel represents a promising therapeutic target to prevent life-threatening arrhythmias induced by acute hypoxia and oxidative stress.
Acute hypoxia is induced during coronary occlusion or when oxygen supply does not meet demand and can trigger cardiac arrhythmia. Cardiac ion channels shape the action potential and excitability of the heart. Acute hypoxia regulates the function of cardiac ion channels including the L-type Ca(2+) channel that is the main route for Ca(2+)influx into cardiac myocytes and shapes the plateau phase of the action potential. This article will review the evidence for alteration of ion channel function during hypoxia as a result of modification of thiol groups by reactive oxygen species. The effect of acute hypoxia on cardiac excitability will be examined and how this can lead to life threatening arrhythmias with particular reference to the L-type Ca(2+) channel. Recent evidence indicates the L-type Ca(2+) channel is a suitable target for the development of drugs that can modify channel function during hypoxia or oxidative stress to prevent induction of arrhythmia or development of pathology.
Macdonald et al. (Mon,) conducted a review in Acute hypoxia and cardiac arrhythmia. L-type Ca(2+) channel targeting was evaluated. Targeting the L-type Ca(2+) channel is a suitable strategy for developing drugs to modify channel function during hypoxia or oxidative stress to prevent induction of arrhythmia.