Autonomic and Neuromuscular Pharmacology Flashcards
Describe the mechanisms by which drugs can modulate synaptic transmission at the neuromuscular junction
Block vesicle fusion or calcium influx, Competitively block ACh receptors (non-depolarizing) or cause prolonged depolarization (depolarizing), Inhibit acetylcholinesterase, increasing ACh levels in the synaptic cleft, Irreversibly inhibit AChE, leading to ACh accumulation, Block sodium channels in nerve endings, Inhibits calcium influx into pres.
Describe the mechanisms by which drugs can modulate synaptic transmission in the
sympathetic and parasympathetic systems.
In summary, drugs modulate sympathetic and parasympathetic synaptic transmission by either enhancing or inhibiting neurotransmitter release, or by acting on specific receptors. Sympathetic drugs often target adverse drug reactions.
Explain the consequences of modulating synaptic transmission in the autonomic ganglia
and the neuromuscular junction.
- Autonomic Ganglia:
- Ganglionic blockers (e.g., hexamethonium) = Reduced sympathetic and parasympathetic activity; hypotension, decreased heart rate, reduced GI motility
- Cholinergic agonists (e.g., nicotine) = Increased sympathetic and parasympathetic activity; tachycardia, hypertension, increased secretions
- Ganglionic toxins (e.g., botulinum toxin) = Impaired autonomic control; flaccid paralysis, loss of autonomic regulation (e.g., blood pressure)
- Neuromuscular Junction (NMJ): AChE inhibitors (e.g., neostigmine, physostigmine) consequence is Enhanced ACh signaling;