Autonomic And Neuromuscular Pharmacology Flashcards
Ganglionic transmission
Drugs can modulate synaptic transmission by inhibiting choline transporter, blocking the V.gated Ca2+ channels, blocking vesicle fusion, non-depolarising nicotinic receptor blockers, depolarising nicotinic receptor blockers, blocking ACh activated channels or by activating nicotinic receptors.
Clinical application of drugs acting during ganglionic trnasmission
Almost none. Drugs modulate sympathetic/parasympathetic transmission and likely NMJ producing complex actions with side effects.
Postganglionic sympathetic transmission
Drugs can modulate synaptic transmission at this stage by blocking NA producing enzymes, blocking the transporter that fills vesicles with NA, introducing a false transmitter, activating inhibitory presynaptic (A2) autoreceptors, blocking A/B post synaptic receptors, stimulating the release of NA, inhibiting the uptake of NA into neurones or by activating postsynaptic receptors.
Clinical applications of altering postganglionic sympathetic transmission
A1 agonists such as decongestants which can dilate the pupil and inhibit secretions.
A2 agonists to treat hypertension.
B2 agonists to treat asthma.
B1 antagonists to treat hypertension, angina, arrhythmias, glaucomas.
Describe the mechansisms by which drugs can modulate synaptic transmission at the NMJ.
Potential sites include inhibition of cholin transport, blocking v.gated Ca2+ channels, blocking the fusion of vesicles (botulinium), non-depolarising nicotinic receptor blockers, depolarising nicotinic receptor blockers, prolonging the AP or blocking acetylcholinesterase.
Clinical applications of drugs which modulate synaptic transmission at the NMJ
(Non)-depolarising blockers are used for temporary paralysis during surgery, ECt or for tetanus spasm.
Botulinium is used for muscle spasms and cosmetics.
Anti-cholinesterase is used for myasthenia gravis, reversing non-depolarising blockers and countering botulinium poisoning.