Kee: Pharmacology, 8th Edition

Chapter 18: Adrenergic Agonists and Adrenergic Blockers

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This chapter discusses two groups of drugs that affect the sympathetic nervous system:
adrenergic agonists (sympathomimetics) and adrenergic blockers (sympatholytics), along with
their dosages and uses.

Drugs that stimulate the sympathetic nervous system are called adrenergics, adrenergic
agonists, or sympathomimetics because they mimic the sympathetic neurotransmitters
norepinephrine and epinephrine. Adrenergic agonists act on one or more adrenergic
receptor sites located in the cells of muscles, such as the heart, bronchiole walls,
gastrointestinal tract, urinary bladder, and ciliary muscle of the eye. The four main
receptors are alpha1, alpha2, beta1, and beta2.
The alpha-adrenergic receptors are located in blood vessels, eye, bladder, and prostate.
When the alpha1 receptors in vascular tissues (vessels) of muscles are stimulated, the
arterioles and venules constrict, increasing peripheral resistance and blood return to the
heart.
The alpha2 receptors are located in the postganglionic sympathetic nerve endings. When
stimulated they inhibit the release of norepinephrine, leading to a decrease in
vasoconstriction.
The beta1 receptors are located in the kidney but primarily in the heart. Stimulation of the
beta1 receptor increases myocardial contractility and heart rate.
The beta2 receptors are found mostly in the smooth muscles of the lung and
gastrointestinal tract, the liver, and the uterine muscle. Stimulation of the beta2 receptor
causes (1) relaxation of the smooth muscles of the lungs, (2) a decrease in gastrointestinal
tone and motility, (3) activation of glycogenolysis in the liver, and (4) relaxation of the
uterine muscle.
Another adrenergic receptor is dopaminergic and is located in the renal, mesenteric,
coronary, and cerebral arteries. When this receptor is stimulated, the vessels dilate, and
blood flow increases. Only dopamine can activate this receptor.
After the neurotransmitter has performed its function, the action must be stopped to
prevent prolonging the effect.
Transmitters are inactivated by (1) reuptake of the transmitter back into the neuron, (2)
enzymatic transformation or degradation, and (3) diffusion away from the receptor.
The two enzymes that inactivate norepinephrine are (1) monoamine oxidase (MAO),
which is inside the neuron, and (2) catechol-O-methyltransferase (COMT), which is
outside the neuron.
Drugs can prolong the action of the neurotransmitter by either (1) inhibiting reuptake,
which prolongs the action of the transmitter, or (2) inhibiting degradation by enzyme
action.
Sympathomimetic drugs are classified into three categories according to their effects on
organ cells. Categories include (1) direct-acting sympathomimetics, which directly
Copyright 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.

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stimulate the adrenergic receptor; (2) indirect-acting sympathomimetics, which stimulate

the release of norepinephrine from the terminal nerve endings, and (3) mixed-acting
sympathomimetics, which stimulate the adrenergic receptor sites and stimulate the release
of norepinephrine from the terminal nerve endings.
Catecholamines are the chemical structures of a substance (either endogenous or
synthetic) that can produce a sympathomimetic response.
Many of the adrenergic agonists stimulate more than one of the adrenergic receptor sites.
Drugs that block the effects of the adrenergic neurotransmitter are called adrenergic
blockers, adrenergic antagonists, or sympatholytics.
Adrenergic blockers act as antagonists to adrenergic agonists by blocking the alpha and
beta receptor sites. Most adrenergic blockers block either the alpha receptor or the beta
receptor. They block the effects of the neurotransmitter either directly by occupying the
receptors or indirectly by inhibiting the release of the neurotransmitters norepinephrine
and epinephrine.
Drugs that block or inhibit a response at the alpha-adrenergic receptor site are called
alpha-adrenergic blockers or alpha blockers. Alpha-blocking agents are divided into two
groups: selective alpha blockers that block alpha1 and nonselective alpha blockers that
block alpha1 and alpha2.
Because alpha-adrenergic blockers can cause orthostatic hypotension and reflex
tachycardia, many of these drugs are not as frequently prescribed as beta blockers.
Alpha blockers can be used to treat peripheral vascular disease. Vasodilation occurs,
permitting more blood flow to the extremities. These drugs are also helpful in decreasing
symptoms of benign prostatic hypertrophy.
Beta-adrenergic blockers, commonly called beta blockers, decrease heart rate, and a
decrease in blood pressure usually follows.
Some of the beta blockers are nonselective, blocking both beta1 and beta2 receptors. Not
only does the heart rate decrease because of beta1 blocking, but bronchoconstriction also
occurs. Nonselective beta blockers (beta1 and beta2) should be used with extreme caution
in any patient who has chronic obstructive pulmonary disease (COPD) or asthma.
Intrinsic sympathomimetic activity (ISA) is the ability of certain beta blockers to bind
with a beta receptor to prevent strong agonists from binding to that receptor producing
complete activation. These agents may be recommended for patients experiencing
bradycardia.
Beta blockers are useful in treating mild to moderate hypertension, angina pectoris, and
myocardial infarction.
Drugs that block the release of norepinephrine from the sympathetic terminal neurons are
called adrenergic neuron blockers, which are classified as a subdivision of the adrenergic
blockers.
The clinical use of neuron blockers is to decrease blood pressure.

Copyright 2015, 2012, 2009, 2006, 2003, 2000, 1997, 1993 by Saunders, an imprint of Elsevier Inc.