Drugs can block autonomic ganglia by any one of several mechanisms. They may act presynaptically by affecting nerve conduction or neurotransmitter synthesis, release, or reuptake. Acting postjunctionally, drugs may affect the interaction between ACh and its receptor, or they may affect depolarization of the ganglion cell or initiation of a propagated action potential.
Ganglionic nicotinic blockers can be divided into two groups. The first group, characterized by nicotine and related drugs (e.g., lobeline, tetraethylammonium), initially stimulates the ganglia and then blocks them (discussed earlier). These agents are not therapeutically useful. The second group of drugs, which have some therapeutic usefulness but are rarely used, inhibit the postsynaptic action of ACh and do not themselves produce depolarization, thereby blocking transmission without causing initial stimulation.
The site of action of many blocking drugs has been shown to be at the associated ionic channel rather than at the receptor. Prolonged administration of ganglionic blocking drugs leads to the development of tolerance to their pharmacological effects.
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