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You are in Home >> Resources >> Pharmacology >> Neuromuscular blockade and reversal

Mechanism of action of neuromuscular blocking drugs

Created: 1/8/2004


General mechanism of action:

Block transmission through the neuromuscular junction (NMJ) at nicotinic receptors, thus decreasing skeletal muscle tone.

NMJ blockers 


Bind to receptors and prevent acetylcholine (Ach) from stimulating receptors
Model = Curare

Effect: compete with Ach for nicotinic receptor binding sites. The blockade is competitive, hence muscle paralysis occurs gradually.

Examples include tubocurarine, gallamine, atracurium, vecuronium, mivacurium, rocuronium  and cisatracurium. These drugs are highly ionised at body pH and contain two quaternary ammonium groups. They are poorly lipid soluble and poorly protein bound.


Produce what appears to be a "persistent" depolarisation of the NMJ. Cause depolarisation by mimicking the effect of Ach but without being rapidly hydrolysed by acetylcholinesterase. Propagation of an action potential is prevented by the area of inexcitability that occurs around the Ach receptors.

Examples include suxamethonium (1951) and decamethonium (1948)
Model = succinylcholine

Action occurs in two phases:

 Phase I - initial brief depolarisation of post-junctional membrane skeletal muscle, thus causing contraction; fasciculations are seen and repolarisation is inhibited

 Phase II-"desensitisation blockade"

After the drug has been present for a period of time, the motor end plate loses its sensitivity and depolarisation cannot occur; desensitisation continues for several minutes, even after drug is no longer present. Depolarising NMJ blockers produce persistent depolarisation = desensitisation

Fasciculations can be prevented by pretreatment with a competitive agent.

Histamine release

This is a feature of tubocurare and succinylcholine (others to lesser extent)

Effects of histamine release:

 dilatation of peripheral blood vessels (decreased blood pressure)
 excessive secretions
 anticoagulant effect

Interactions of NMJ blockers 

Blockade is potentiated with general inhalational anaesthetics; antibiotics, e.g. gentamycin (decrease Ach release) and tetracyclines (chelate calcium and decrease Ach release).
Blockade is reduced with anticholinesterase agents. Results in increased Ach levels at the NMJ, thus antagonising the effects of competitive agents.

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