Site of action of vecuronium is?
Ans. is 'd' i.e., Neuro-muscular junction* Vecuronium, a non-depolarizing blocker, acts on nicotinic receptors at myoneural junction.* Neuro-muscular blocker act at myoneural junction1. Competitive (Non-depolarizing) blocker: -# They compete with Achfor Nm receptors - called competitive blockers. They prevent binding of Ach to Nm receptors - No opening of Na+ channels - No depolarization, so these are called non-depolarizing blockers. Competitive blockers reduce the frequency of channel opening but not its duration or the conductance of a channel once it has opened. When the magnitude of end plate potential falls below a critical level, it is unable to trigger propagated muscle action potential - muscle fails to contract. Neostigmine (anticholinesterases) antagonises competitive blockers as it increases the concentration of Ach by inhibiting its degradation by cholinesterase. Therefore, Neostigmine is used for the reversal of competitive (nondepolarizing) blockers.2. Depolarizing blockers (Succinylcholine, Decamethonium)# Depolarizing blockers have affinity as well as submaximal intrinsic activity on NM receptors. They depolarize muscle end plates by opening of Na+ channels and initially produce twitching and fasciculations (not full contraction as these drugs have submaximal activity) - So, they are called depolarizing blocker. These drugs do not dissociate rapidly from the receptor (NM) - Persistant partial depolarization - Na+ channels get inactivated - flaccid paralysis. Neostigmine does not antagonize depolarising blockers (Therefore neostigmine cannot be used for reversal).Inf act neostigmine can potentiate the block as neostigmine and other anti-cholinesterase also inhibits pseudocholinesterase which metabolizes Sch.Under certain conditions depolarizing agents produce dual mechanism of neuromuscular blockade which can be divided into two phases :a) Phase I block* Rapid in onset* Result from persistant depolarization of muscle end plate - Typical mechanism of action of depolarizing blocker.* Has classical features of depolarization block.* Block is not antagonized by anticholinesterases (neostigmine).b) Phase II block (Dual block)* Slow in onset* Results from desensitization of receptor to ACh - Ach can not act on Nm receptors (similar to competitive blocker).* Resembles block produced by competitive blockers - Therefore, has characteristics similar to non-depolarizing (competitive) block.* Block is partially reversed by anticholinesterases (Neostigmine).# In man, normally, only phase I block is seen - typical depolarizing block.# Phase II block is seen when fluorinated anaesthetics have been given or when SCh is injected in high dose.# SCh also produces phase II block in patients with atypical or deficient pseudocholinesterase.
Cerebrum
Reticular formation
Motor neuron
Neuro-muscular junction
Muscle Relaxant