Calcium channel blocker: NM blockade
Last updated: 05/30/2013
Calcium channel blockers are among the list of drugs found to prolong neuromuscular blockade (others include: aminoglycosides, tetracyclines, polymyxins, anticholinesterases, local anesthetics, and volatile anesthetics).
There are two types of calcium channels that seem to be important for release of neurotransmitter: P channels and L channels. Slower L-type channels found in the cardiovascular system are profoundly affected by calcium channel blocking drugs such as verapamil, diltiazem and nifedipine. P channels are only found in synaptic nerve terminals and are thought to be responsible for normal release of neurotransmitter. P channels are not directly affected by L-type calcium channel blockers so these drugs do not significantly affect normal acetylcholine release at nerve terminals or strength of neuromuscular transmission. However, there is data to suggest that calcium channel blockers may prolong neuromuscular blockade caused by non-depolarizing muscle relaxants. This could be explained by the fact that nerve terminals also contain L-type channels. Another explanation is that calcium channel blockers may cause allosteric inhibition of calcium channels, meaning more channels are in the desensitized state leading to a decreased efficacy of neuromuscular transmission and greater susceptibility to neuromuscular blockade by muscle relaxants.
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