Sodium channel blocker

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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(e) Sodium channel antagonist; Sodium channel antagonist; Sodium channel blocker

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Sodium channel blockers are a group of drugs whose mechanism of action consists in the antagonization of voltage-dependent or non-voltage-dependent sodium channels.

Voltage-dependent sodium channels initiate action potentials by intracellularly directed depolarization currents in neurons and cardiomyocytes. Accordingly, NAV antagonists inhibit neuronal or cardiac excitability (see also ion channels).

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The following substance groups function by blocking voltage-dependent Na+ channels:

Local anaesthetics are substances that reversibly block the initiation and transmission of action potentials in nerve fibres by blocking voltage-dependent Na+ channels. They are divided according to their chemical structure into:

  • Local anaesthetics of the ester type

  • Amide-type local anaesthetics

Anticonvulsants (antiepileptic drugs) whose essential mechanism of action is seen in a blockage of the sodium channel (e.g. carbamazepine, felbamate, lamotrigine, oxcarbazepine, phenytoin or topiramate).

Antiarrhythmics (Class I antiarrhythmics): Their main representatives include ajmaline, quinidine, flecainide, lidocaine, prajmaline and propafenone. They inhibit the rapid influx of sodium (by directly blocking the voltage-dependent Na+ channels) of phase I of the action potential in the working myocardium. These can be divided according to their binding behaviour into:

  • Fast-Drugs: They quickly release themselves from the Na+ channel. These include lidocaine and tocainide.

  • Slow-Drugs: They are released from the Na+-channel with a significant delay (all other antiarrhythmic drugs).


Last updated on: 29.10.2020