Exam #1
Adrenergic Drugs
(Sympathetic Nervous
System)
The neurotransmitters involved in adrenergic drugs are catecholamine’s (norepinephrine,
epinephrine, and dopamine). There are receptor sites for the catecholamine’s norepi and epi
throughout the body and are referred to as adrenergic receptors.
Adrenergic receptors
Alpha-adrenergic
o Alpha1
Located on postsynaptic effector cells (cell, muscle, or organ that nerve
stimulates)
o Alpha2
Located on presynaptic nerve terminals (nerve that stimulates the effector
cells)
Controls the release of neurotransmitters
o Alpha-Adrenergic Agonist
Vasoconstriction
CNS Stimulation
Beta-adrenergic are all located on postsynaptic effector cells
o Beta1
Located primarily in the heart
o Beta2
Located in the smooth muscle of bronchioles, arterioles, and visceral
organs
o Beta-Adrenergic Agonist
Bronchial, gastrointestinal, and uterine smooth muscle relaxation
Glycogenolysis
Cardiac stimulation
Dopaminergic
o Causes dilation of the following blood vessels resulting in increased blood flow
Mechanism of action
Direct-Acting
o Binds directly to the receptor and causes a physiologic response
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Indirect-Acting
o Causes release of catecholamine from storage sites in nerve endings
o Catecholamine binds to receptors and causes a physiologic response
Mixed-Acting
o Directly stimulates the receptor by binding to it and indirectly stimulates the
receptor by causing the release of stored catecholamine’s from the nerve endings
Stimulation of alpha-adrenergic receptors on smooth muscles results in:
Vasoconstriction of blood vessels
Relaxation of GI smooth muscles (decreases motility)
Constriction of balder sphincter
Contraction of uterus
Male ejaculation
Contraction of pupillary muscles of eye (dilated pupils)
Stimulation of beta1-adrenergic receptors on the myocardium, AV node, and SA node results in
cardiac stimulation
Increased force of contraction (positive inotropic effect)
Increased heart rate (positive chronotropic effect)
Increased conduction through the AV node (positive dromotropic effect)
Stimulation of beta2-adrenergic receptors on the airways results in
Bronchodilation (relaxation of the bronchi)
Uterine relaxation
Glycogenolysis the liver
Increased renin secretion in the kidneys
Relaxation of GI smooth muscles (decreased motility)
Indications
Respiratory Indications
Beta2-adrenergic receptors and cause bronchodilation. Beta2 agonists are helpful in
treating conditions such as asthma and bronchitis.
Indications of Topical Nasal Decongestants
Treatment for nasal congestion, stimulate alpha1-adrenergic receptors and have little or no
effect on beta-adrenergic receptors
Ophthalmic Indications
Stimulate alpha-adrenergic receptors located on small arterioles in the eye and
temporarily relieve conjunctival congestion by causing arteriolar vasoconstriction.
Temporary relief of conjunctival congestion
Reduction of intraocular pressure and dilation of pupils
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Cardiovascular Indications
Used to support the heart during cardiac failure or shock
Contraindications
Drug allergy
Severe hypertension
Adverse Effects
Alpha-Adrenergic
o CNS
Headache, restlessness, excitement, insomnia, euphoria
o Cardiovascular
Palpitations, tachycardia, hypertension
o Other
Loss of appetite, dry mouth, N/V
Beta-Adrenergic
o CNS
Mild tremors, headache, nervousness, dizziness
o Cardiovascular
Elevated heart rate, palpitations, fluctuations in blood pressure
o Other
Sweating, N/V/, muscle cramps
Toxic Effects
Seizures, hypotension, hypertension, dysrhythmias, palpitations, nervousness, dizziness, fatigue,
malaise, insomnia, headache, tremor, dry mouth, nausea
Interactions
Adrenergic antagonist (compete and limit therapeutic effect)
Anesthetics (increases risk for cardiac dysrhythmias)
MAOI (may cause hypertensive crisis b/c increase levels of norepi and dopamine)
Antihistamines and thyroid preparations increase effects of adrenergic drugs
Lab interactions
↑ corticotrophin levels
↑ corticosteroids
↑ glucose
Dobutamine (Beta1-selectve vasoactive adrenergic drug)