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Home Books Katzung & Trevor's Pharmacology: Examination & Board Review, 11e

Chapter 6: Introduction to Autonomic Pharmacology

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?

(A) Bronchodilation

(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.

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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

aToxin of puffer fish, California newt.

bToxin of Gonyaulax (red tide organism).

cNorepinephrine, dopamine, acetylcholine, angiotensin II, various prostaglandins, etc.

dToxin of marine snails of the genus Conus.

eBlack widow spider venom.

Modified and reproduced, with permission, from Katzung ...

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