2. Cholinergic receptors: Nicotinic receptors & Muscarinic receptors
Present in Autonomic ganglia (NN) Adrenal medulla (NN) Motor endplate
(NM) CNS (Spinal cord mainly) (NN)
Present in Effector organ supplied by Parasymp Sweat glands BV CNS
(Brain Mainly)
Blocked By Ganglion blocker (Nicotine, LD, in ganglia) Neuromucular
blocker (eg. Curare in skeletal muscles) Blocked by Atropine
3. Neuromuscular Blockers
Ganglion and Neuromuscular Junction blockers
• Look like acetylcholine
• Either work as antagonists or agonists
• Two classes:
• Non-depolarizing (antagonist)
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.
• Eg: tubocurarine
• Block ion channels at motor end plate
• Depolarizing (agonist)
These agents act by depolarizing the skeletal muscle fiber. This persistent depolarization
makes the muscle fiber resistant to further stimulation by ACh.
• Eg: succinylcholine
• Activates receptor
4. Competitive non-depolarizing
• Non-depolarizing blockers are reversed by acetylcholinesterase inhibitor drugs since non-
depolarizing blockers are competitive antagonists at the ACh receptor sites.
Non competitive depolarizing
• Depolarizing blocking agents acts by depolarizing the plasma membrane of the muscle fiber, similar
to acetylcholine. These agents are more resistant to degradation by acetylcholinesterase.
Neuromuscular Blockers
5. Ganglion blocking drugs
• They inhibit transmission between preganglionic and postganglionic neurons in the autonomic
nervous system. Examples are, Hexamethonium, gallamine, pentolinium, mecamylamine,
trimetaphan, tubocurarine, chlorisondamine, pentaamine.
They are mostly Nicotinic receptor agonists acting through depolarization block
NB: Botulinum toxin blocks ACh release in autonomic ganglia
Neuromuscular Blockers
6. DRUGS AFFECTING GANGLIA (Ganglion blockers)
• Depolarizing ganglion blockers - Produce initial stimulation then block (Nicotine large dose)
(Competitive ganglion blocker)
• Quaternary amines, Hexametonium and chlorisondamine
• Secondary amine (Mecamylamine), Trimetaphan (short acting histamine liberator,
by I.V., No CNS effects)
Actions
• Effects like atropine
• Postural hypotension
• Impotence
Uses
• Trimetaphan used in hypertensive emergency, to induce controlled hypotension in surgery
Neuromuscular Blockers
7. Neuromuscular Junction blocking drugs
They block neuromuscular transmission at the neuromuscular junction, causing
paralysis of the affected skeletal muscles. This is accomplished via their action on
the post-synaptic acetylcholine (Nm) receptors.
Depolarizing blocking agents
Non-depolarizing blocking agents
Neuromuscular Blockers
8. Act by blocking effects of ACh at the skeletal NMJ (Competitive non-depolarizing agents) e.g
Gallamine, Pancuronium, they compete with ACh for nicotinic receptors at the
NMJ. EPP, depolarization threshold is not reached
Uses
• Promote skeletal muscle relaxation
• Promote endotracheal intubation
• Adjunct to surgical anesthesia
• Limit trauma due to Electroconvulsive shock
Adverse effects
• Respiratory paralysis
• Histamine release
• Bronchospasm
• hypotension
9. • Act by blocking effects of ACh at the skeletal NMJ (Non-competitive depolarizing agents), e.g
succinylcholine, decamethonium
• Desensitize the nicotinic receptors at NMJ, receptor sensitivity
Uses
• Promote sk muscle relaxation
• Promote endotracheal intubation
• Adjunct to surgical anesthesia
• Limit trauma due to Electroconvulsive shock
Adverse effects
• Respiratory paralysis
• Muscle fasciculation and pain
• Increased IOP
• Bradycardia (muscarinic effect)
10. Make a list of 20 neuromuscular blocking agents and classify they as depolarizing
and non depolarizing ganglion or neuromuscular junction blockers.
