Pharmacology · Class
Neuromuscular blockers !
They paralyse skeletal muscle at the motor end plate for intubation and surgery. They neither sedate nor relieve pain: always with anaesthesia.
Updated 2026-11-01
What they are
Drugs that block transmission at the neuromuscular junction. Suxamethonium is depolarising (very fast onset, effect of minutes). Non-depolarising agents compete with acetylcholine: aminosteroids (rocuronium, vecuronium, pancuronium) and benzylisoquinolines (atracurium, cisatracurium).
Mechanism of action
They act on the muscle nicotinic receptor of the motor end plate. Suxamethonium activates it like acetylcholine, depolarises the end plate (fasciculations) and leaves it unable to respond while it persists (phase I block). Non-depolarising agents occupy the acetylcholine site without opening the channel; their block is reversed by raising acetylcholine (neostigmine) or, for rocuronium and vecuronium, by trapping the molecule with sugammadex.
Target: Muscle nicotinic acetylcholine receptor (motor end plate)
Drugs in this class
- SuxamethoniumDepolarising muscle relaxant with onset in under a minute and an effect of a few minutes, for rapid intubation. It can…Muscle nicotinic acetylcholine receptor (motor end plate)
- RocuroniumNon-depolarising muscle relaxant with fast onset and intermediate duration. Sugammadex reverses it even from a deep…Muscle nicotinic acetylcholine receptor (motor end plate)
- VecuroniumIntermediate-acting non-depolarising aminosteroid muscle relaxant that releases no histamine. Sugammadex reverses it.Muscle nicotinic acetylcholine receptor (motor end plate)
- AtracuriumNon-depolarising muscle relaxant that breaks down by itself in the blood (Hofmann elimination): useful in liver or…Muscle nicotinic acetylcholine receptor (motor end plate)
- CisatracuriumAn isomer of atracurium, more potent and without histamine release. Eliminated by Hofmann degradation, independent of…Muscle nicotinic acetylcholine receptor (motor end plate)
- PancuroniumLong-acting aminosteroid muscle relaxant, the prototype of the group. Its vagolytic effect causes tachycardia; it is…Muscle nicotinic acetylcholine receptor (motor end plate)
Others in the class
- Mivacurium
- Tubocurarine
Test yourself
Think of the answer, then tap the question to see it.
Why does suxamethonium cause fasciculations?
Because it activates the nicotinic receptor and depolarises the end plate before leaving it unresponsive.
What is the main difference in action between suxamethonium and rocuronium?
Suxamethonium depolarises the end plate (agonist); rocuronium competes with acetylcholine without activating the receptor (competitive antagonist).
Why does suxamethonium cause severe hyperkalaemia days after an extensive burn or denervation?
The muscle expresses many nicotinic receptors outside the end plate; activating them all at once releases a large amount of potassium from the cells.
What simple signs of recovery are sought before extubating a patient who received a blocker?
An adequate train-of-four response and clinical signs such as a sustained head lift, good phonation and adequate ventilation.
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed., ch. 13 (McGraw Hill, 2023); DailyMed - SUCCINYLCHOLINE CHLORIDE injection, solution (DailyMed (U.S. National Library of Medicine), 2026); DailyMed - ROCURONIUM BROMIDE injection, solution (DailyMed (U.S. National Library of Medicine), 2026); Malignant hyperthermia: MedlinePlus Genetics (MedlinePlus (U.S. National Library of Medicine), 2026).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.