Adrenergic
Adrenergic Agonists
Catecholamines
Endogenous
Epinephrine
MOA: Released by Adrenal Medulla, agonist
at both a and B receptors (a1=a2; B1-B2)
Clinical: Bronchospasms, Anaphylactic
Shock, Cardiac Arrest, Anesthetic adjunct (
prolongs duration of action)
Increases cardiac output (increase SBP with
minimal decrease in DBP), Bronchodilation.
At lower Dose: B2 vasodilation
predominates, higher Dose: a1
vasoconstriction predominates
Adverse: CNS, anxiety, fear, tremor /
Cardiac (HTN, Tachyarrhythmias), / Cerebral
Hemorrhage / Mydriasis / Hyperglycemia /
Extravasation-tissue necrosis
Dipivefrin
MOA: Prodrug metabolized to Epinephrine in
the eye that decreases IOP by contract radial
muscle that opens trabecular network to
increase aqueous humor outflow
Clinical: Open-angle Glaucoma
Adverse: Mydriasis / Burning & Stinging
NorEpinephrine
MOA: Agonist at both a and B receptors (a
effects >> B1>>B2) / Increased
vasconstriction and increases inotropic
effect (rate-neutral due to reflex
Bradycardia) to increase BP
Clinical: short-term Tx of shock (
Hypotension)
Arrhythmia: Dopamine>>NorEpinephrine; no
mortality difference
Adverse: CNS (anxiety, fear, tremor),
Cardiac (HTN), Cerebral Hemorrhage (2nd
increase BP), Extravasation-tissue necrosis
Interactions: a-blockers (Physiological
Antagonism) B-blockers (Exaggerated a
response), Increase efficacy: MAO-inhibitor
and COMT inhibitor
Dopamine
MOA: Stimulates a, B, and Dopamine (D)
receptors depending on dose- a-receptors
increase BP at higher doses, B-receptors
increase cardiac output (increase SBP with
minimal to DBP), D-receptors may increase
Renal perfusion increasing diuresis
Clinical: Critical Care- low to moderate dose
for Cardiac and Septic Shock
Alternative to NE, Arrhythmia: Dopamine>>
NE: no mortality difference, Low dose D
should NOT be used for Renal protection
Monitor: ECG, Vitals, Urine output
Adverse: CNS, anxiety, fear, tremor /
Cardiac (HTN, Tachyarrhythmias), / Cerebral
Hemorrhage / Mydriasis / Hyperglycemia /
Extravasation-tissue necrosis
Interactions: a-blockers (physiological
antagonism), B-blockers (exaggerated a-
response), Increase efficacy: MAO-inhibitors
and COMT inhibitors
Adrenergic Antagonist >>>
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Direct-Acting Agonist Indirect Acting Agonist Mixed Action Agonist
Bind directly with Adrenergic receptors Non-Catecholamines Bind directly with Adrenergic receptors and
Facilitate release (displacement) of NE or displace NE from storage sites
inhibit reuptake of NE
Synthetic
B2-Agonists (-ol) Dextoamphetamine / Methamphetamine
Ephedrine / Ephedra
Isoproternol MOA: Relaxes Bronchial smooth muscle
resulting in Bronchodilation MOA: Causes release oc Catecholamines (NE,
5HT, D) from pre-synaptic storage sites, MOA: direct acting a and B-agonist, also
inhibits their reuptake displaces NE from storage site
MOA: Non-selective agaonist at B1 and B2 Clincal: Asthma, COPD
receptors (B1=B2) Clinical: ADHD, Narcolepsy, Obesity, Clinical: Ephedrine (1) Bronchospasms, (2)
Depression Nasal congestion, (3) HTON - temporarily
relieves SOB, tightness of chest and
Stimulates HR and contractility to maintain Monitor: Peak Expiratory Flow Rate (PEFR)
wheezing due to bronchial asthma
cardiac output (B1 stimulation increases SBP; and Pulmonary Function Tests (PFT) Adverse: CNS (insomnia, irritability, tremor,
B2 stimulation decreases DBP), while also confusion, panic state, suicidal tendiencies,
causing Bronchodilation amphetamine psychosis / Dependence / HTN, Clinical: Ephedra: (1) Weight loss, (2) Energy
palpations / GI (NVD, anorexia) / Decreaseed booster, (3) Enhance Athletic performance
Adverse: Cardiac (increase BP, Tachycardia),
growth rate (peds)
Clinical: Bradyarrhythmias; Temporary use in CNS Stimulation (nervousness, restlessness),
3rd Degree AV block until Pacemaker Hypokalemia, Hyperglycemia Adverse: CNS (anxiety, insomnia), CV (HTN,
insertion Contraindication: Pts with HTN, CV disease, Tachycardia), may interfere with detection
Hyperthyroidism, Glaucoma of amphetamines (false-positive)
Monitor: ECG Interactions: B-blockers (primarily non-
selective Interactions: MAO-Inhibitors Interactions: a-blockers
Adverse: CNS (anxiety, fear, tremor),
Cardiac (Tachyarrhythmias), Hyperglycemia Tyramine Pseudophedrine
Short-Acting B2-Agonist Long-Acting B2-Agonist
Interactions: COMT inhibitors may prolong
action, B-blockers result in physiologic
antagonism Drug Interactions! = not marketed MOA: Direct acting a and B-agonist (a>B)
Albuterol Arformoterol while also displacing NE from storage site
Dobutamine MOA: enters nerve terminals and displaces
NE, which then acts on a-receptors Clinical: Relief of Nasal congestion
DOC for acute (or rescue) Respiratory relief ( Approved for COPD only
COPD, Asthma) Found in fermented foods Adverse: Cardiac (HTN, Tachycardia),
MOA: Selective B1 agonist, Increase strength Illegally used as precursor to
of contraction (rate neutral) increase cardiac Formoterol methamphetamine, May interfere with urine
Levalbuterol Pts taking a mono amine oxidase inhibitors (
output (SBP increase) detection of amphetamine (false-positive)
MAOI) who eat Tyramine containing foods
can develop HTN crisis
Clinical: Increase Cardiac Output in Acute Interactions: a-blockers
Possesses a rapid onset (5 mins: 80% peak
Decompensated Heart Failure (ADHF)
R-isomer of Albuterol, purported to cause effect in 15 min) not approved for acute Cocaine (Class II)
fewer side effects relief of asthmatic symptoms
Monitor: ECG
Metaproterenol Salmeterol
Adverse: CNS (Headache), Cardiac (A-fib) MOA: Inhibits reuptake of NE/EPI back into
synaptic vesicles, blocks initiation or
Terbutaline
conduction of the nerve impulse following
Interactions: COMT inhibitors may prolong local application
action, B-blockers result in physiologic Onset: 30 min for Asthma, 2 hrs for COPD
antagonism
Rarely used as Bronchodilator; Primarily used Indacterol Clinical: Topical anesthesia to accessible
to suppress Premature Birth mucouse membranes of oral, laryngeal, and
nasal cavities
Approved for COPD only Adverse: CNS stimulation/depression,
Cardio: Bradycardia (low dose),Tachycardia (
high dose), Vasoconstriction
Phenylephrine
Fatal Overdose: appx 1.2 gm; severe toxic
effects at even 20 mg
MOA: Synthetic a1-agonist, Increases BP,
Dilates Pupil, constricts engorged ocular,
nasal, and rectal vasculature to decrease
redness and congestion, shrinks hemorrhoids
Clinical: Tx of Hypotension/vascular failure
2nd to Shock, Mydriatic for EYE procedures,
Relief of eye redness, Hemorrhoids, and
Nasal congestion
Monitor: Increased BP
Adverse: Exravasation (IV)-tissue necrosis,
Hypertensive HA, Hypertensive patients,
Rebound congestion (nasal >3-5 days)
Interactions: a-blockers, MAO-inhibitors
Oxymetazoline
MOA: a1 and a2 agonist, EYE drops or Nasal
spray produce vasoconstriction that
decreases blood flow resulting in decreased
ocular redness and nasal congestion
Clinical: Ocular and Nasal vasoconstrictor (
relief of redness and congestion)
Adverse: Rebound hyperemia/congestion,
Ocular stinging/burning
Midodrine
MOA: Prodrug that forms an active
metabolite, Desglymidodrine, an a1-agonist,
Causes vasoconstriction, increase BP
Clinical: Tx of symptomatic orthostatic
hypotension
Adverse: HTN, Bradycardia, Piloerection (
Goose bumps), Paresthesia (Skin sensations,
burning, prickling, itching, tingling)
Interactions: MAO-inhibitors
Clonidine
MOA: Stimulates a2 presynaptic receptors in
the brain stem (Central), Reduces
sympathetic outflow from CNS and
decreases Peripheral resistance, Renal
vascular resistance, HR, and BP
Clinical: HTN, ADHD (peds), Tourette (off-
label), Opioid withdrawal (off-label),
Nicotine withdrawal (off-label)
Caution: Do not discontinue long-term
Clonidine use suddenly
Adverse: CNS, Anticholinergic, Skin reactions
with transdermal, Sodium + Water retention,
may be given with diuretic
Interactions: May enhance AV-blocking
effect of B-blocker, Closely monitor HR
during treatment with B-blocker and
Clonidine. Withdraw B-blocker several days
before clonidine withdrawal, monitor BP
Brimonidine
MOA: Ocular a2-agonist, decreases aqueous
humor production
Clinical: Tx Glaucoma
Adverse: Ocular burning/stining
Mirabegron
MOA; B3-agonist that relaxes detrusor
muscle, increases bladder capacity
Clinical: Overactive bladder with symptoms
of urge urinary incontinence, urgency and
frequency
Adverse: Increase BP
Interactions: Anticholinergics for the
bladder (increases urinary retention)
Fenoldopam
MOA: D1-agonist binds with moderate
affinity to a2-receptors, Rapid acting
vasodilator, Decreases peripheral vascular
resistance and BP secondary to increased
renal blood flow, and natriuresis/diuresis
Clinical: Tx in Hospital, short-term (48hrs)
mgmt of Severe HTN, 6x more potent as
Dopamine in producing Renal Vasodilation
Adverse: HA, flushing, dizziness, N/V,
Tachycardia, Hypokelemia