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Non-depolarizing blockers are reversed by acetylcholinesterase inhibitor drugs since non-depolarizing blockers are competitive antagonists at the ACh receptor so can be reversed by increases in ACh. The depolarizing blockers already have ACh-like actions, so these agents have prolonged effect under the influence of acetylcholinesterase inhibitors.
Non-depolarizing neuromuscular blockers: Non-depolarizing agents act as competitive inhibitors for acetylcholine. Upon the binding of non-depolarizing neuromuscular blockers, neurotransmission is reduced. [1] Consequently, depolarizing and muscle-contracting effects are decreased.
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.
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]
Rocuronium bromide is a competitive antagonist for the nicotinic acetylcholine receptors at the neuromuscular junction. Of the neuromuscular-blocking drugs it is considered to be a non-depolarizing neuromuscular junction blocker, because it acts by dampening the receptor action causing muscle relaxation, instead of continual depolarisation which is the mechanism of action of the depolarizing ...
The change in charge typically occurs due to an influx of sodium ions into a cell, although it can be mediated by an influx of any kind of cation or efflux of any kind of anion. The opposite of a depolarization is called a hyperpolarization.
According to their site of actions, cholinergic blocking drugs can be classified into two general types — antimuscarinic and antinicotinic agents. [1] Antimuscarinic agents (also known as muscarinic antagonists), including atropine and hyoscine, block acetylcholine at the muscarinic acetylcholine receptors.
Its action leads to the accumulation of acetylcholine in the neuromuscular junction that compete with the non-depolarizing blocker agent bound to the acetylcholine receptors. By interfering with the breakdown of acetylcholine, neostigmine indirectly stimulates both nicotinic and muscarinic receptors. [10]