U-50,488H, a kappa opioid receptor agonist, is a more potent blocker of cardiac sodium channels than lidocaine.

Voltage-gated sodium channels are responsible for the initial rapid membrane depolarization phase of the action potential and the genesis of conducting action potentials. The channels can transition between at least three distinct states: resting (closed), open (active) and inactive (nonconducting) [1]. The transitions between these states are voltage and time-dependent. Different sodium channels are expressed in different tissues, there being at least 9 distinct but homologous mammalian sodium channel isoforms [2]. In cardiac tissue, the action of antiarrhythmic drugs such as lidocaine is to prevent abnormal electrical impulse propagation and conduction, thus suppressing non-pacemaker generated electrical activity that results from damage to cardiac myocytes. Class I antiarrhythmic drugs suppress the propagation of cardiac impulses by interacting differentially with the states of the sodium channel [3].