Chapter 6: Introduction to Autonomic Pharmacology
A 3-year-old child has been admitted to the emergency department having swallowed the contents of 2 bottles of a nasal decongestant. The active ingredient of the medication is a potent, selective α-adrenoceptor agonist drug. Which of the following is a sign of α-receptor activation that may occur in this patient?
(B) Cardiac acceleration (tachycardia)
(C) Pupillary dilation (mydriasis)
(D) Renin release from the kidneys
(E) Vasodilation of the blood vessels of the skin
Mydriasis can be caused by contraction of the radial fibers of the iris; these smooth muscle cells have α receptors. All the other listed responses are mediated by β adrenoceptors (Table 6–4). The answer is C.
TABLE 6–4: Steps in autonomic transmission: effects of drugs.
|Process ||Drug Example ||Site ||Action |
|Action potential propagation ||Local anesthetics, tetrodotoxin,a saxitoxinb ||Nerve axons ||Block sodium channels; block conduction |
|Transmitter synthesis ||Hemicholinium ||Cholinergic nerve terminals: membrane ||Blocks uptake of choline and slows synthesis of acetylcholine |
| ||Alpha-methyltyrosine (metyrosine) ||Adrenergic nerve terminals and adrenal medulla: cytoplasm ||Slows synthesis of norepinephrine |
|Transmitter storage ||Vesamicol ||Cholinergic terminals: vesicles ||Prevents storage, depletes |
| ||Reserpine ||Adrenergic terminals: vesicles ||Prevents storage, depletes |
|Transmitter release ||Manyc ||Nerve terminal membrane receptors ||Modulates release |
| ||ω-Conotoxin GVIAd ||Nerve terminal calcium channels ||Reduces release |
| ||Botulinum toxin ||Cholinergic vesicles ||Prevents release |
| ||Alpha-latrotoxine ||Cholinergic and adrenergic vesicles ||Causes explosive release |
| ||Tyramine, amphetamine ||Adrenergic nerve terminals ||Promotes release |
|Transmitter uptake after release ||Cocaine, tricyclic antidepressants ||Adrenergic nerve terminals ||Inhibit uptake; increase transmitter effect on postsynaptic receptors |
| ||6-Hydroxydopamine ||Adrenergic nerve terminals ||Destroys the terminals |
|Receptor activation or blockade ||Norepinephrine ||Receptors at adrenergic junctions ||Binds α receptors; causes activation |
| ||Phentolamine ||Receptors at adrenergic junctions ||Binds α receptors; prevents activation |
| ||Isoproterenol ||Receptors at adrenergic junctions ||Binds β receptors; activates adenylyl cyclase |
| ||Propranolol ||Receptors at adrenergic junctions ||Binds β receptors; prevents activation |
| ||Nicotine ||Receptors at nicotinic cholinergic junctions (autonomic ganglia, neuromuscular end plates) ||Binds nicotinic receptors; opens ion channel in post-synaptic membrane |
| ||Hexamethonium ||Ganglionic nicotinic receptors ||Prevents activation of NN receptors |
| ||Tubocurarine ||Neuromuscular end plates ||Prevents activation of NM receptors |
| ||Bethanechol ||Parasympathetic effector cells (smooth muscle, glands) ||Binds and activates muscarinic receptors |
| ||Atropine ||Parasympathetic effector cells ||Binds muscarinic receptors; prevents activation |
|Enzymatic inactivation of transmitter ||Neostigmine ||Cholinergic synapses (acetylcholinesterase) ||Inhibits enzyme; prolongs and intensifies transmitter action |
| ||Tranylcypromine ||Adrenergic nerve terminals (monoamine oxidase) ||Inhibits enzyme; increases stored transmitter pool |
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