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Non-depolarizing blocking agents: These agents constitute the majority of the clinically relevant neuromuscular blockers. They act by competitively blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors.
Consequently, depolarizing and muscle-contracting effects are decreased. Non-depolarizing neuromuscular blockers are generally reversible, and hence have no permanent effects on acetylcholine receptors. [1] [4] Unlike depolarizing neuromuscular blockers, non-depolarizing drugs do not produce conformational changes to the receptor. [1]
Alternatively, depolarizing agents, such as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction. [5]
Non-depolarizing neuromuscular blocking agents (i.e. Rocuronium, Vecuronium) interact with Ach receptor without activating the channel, as well as preventing the binding of acetylcholine to it. This blocks the signal propagation from the presynaptic neuron, and the severs the transduction of the excitatory signal from the synaptic cleft.
Paralytics are also known as neuromuscular-blocking drugs (NMB). NMB can reduce the complication rates of rapid sequence induction such as inadequate oxygenation of the blood, airway complications, and instability of the cardiovascular system. NMB can be divided into two types: depolarising and non-depolarizing blockers. [18]
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