The action of administered acetylcholine on effector systems innervated by parasympathetic postganglionic neurons (smooth muscle cells, cardiac muscle cells, and exocrine gland cells) resembled the actions produced by the naturally occurring plant alkaloid muscarine. The actions of both acetylcholine and muscarine on the visceral effectors are similar to those produced by parasympathetic nerve stimulation. Furthermore, the effects of acetylcholine, muscarine, and parasympa-thetic nerve stimulation on visceral effectors are antagonized by atropine, another plant alkaloid.
The administration of acetylcholine mimics the stimulatory effect of nicotine, the alkaloid from the tobacco plant, on autonomic ganglia and the adrenal medulla. It has become common practice to refer to the effects of acetylcholine on visceral effectors as the mus-carinic action of acetylcholine and to its effects on the autonomic ganglia and adrenal medulla as the nicotinic action of acetylcholine. The respective receptors are called the muscarinic and nicotinic cholinoreceptors or the muscarinic and nicotinic receptors of acetylcholine.
The action of acetylcholine at the skeletal muscle motor end plate resembles that produced by nicotine. Thus, the cholinoreceptor on skeletal muscle is a nico-tinic receptor. Based on antagonist selectivity, however, the autonomic and somatic nicotinic receptors are not pharmacologically identical (see Chapter 14).
Acetylcholine can stimulate a whole family of receptors. However, these receptors are sufficiently chemically diverse that different exogenous agonists and antagonists can distinguish among them. Great therapeutic benefit has been obtained from this diversity because it allows the development of therapeutic agents that can selectively mimic or antagonize actions of acetylcholine. Such a diversity of receptor subtypes exists for other neurotransmitters in addition to acetyl-choline.
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