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Inhibits Tyrosine hydroxylase Used to treat pheochromocytoma |
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Inhibits AAAd (DOPA decarboxylase) Used to treat Parkinson's Does not cross the blood brain barrier |
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Inhibits Monoamine Oxidase-B Used to treat Parkinson's |
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Inhibits Dopamine β-hydroxylase, DBH (Cu-chelator) is used to treat alcoholism |
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Mechanism: Permanently inhibits amine-H+ exchanger in vesicular membranes needed for catecholamine packaging, can cross the BBB End Effect: Depletes catecholamine stores Use: Hypertension, psychosis
SE: Depression, GI hemorrhage, diarrhea, nasal stuffiness
Note: “Hit and run”, action of drug much longer than plasma half-life |
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Mechanism: α2 receptor agonist, inhibits release of catecholamine-containing vesicles in the CNS End Effect: Reduces catecholamines in the synapse
Use: Hypertension therapy (w/ renal issues due to CNS action), SE: Dry mouth, somnolence, |
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Mechanism: 1) Blocks release of packaged catecholamines, 2) requires Uptake 1 to enter nerve terminal and inhibits it based on competition, does not cross the BBB End Effect: Depletes catecholamine stores Use: Hypertension SE: Postural hypotension |
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Mechanism: 1) Displaces catecholamines out of the nerve terminal, 2) requires Uptake 1 to enter nerve terminal and inhibits it End Effect: Increases catecholamines in the synapse SE w/ MAOIs: Hypertensive crisis, “Cheese Syndrome”
Note: Found in some wine, cheeses, pickled meats, chocolates, alcoholic beverages, fruits, and vegetables
Usually metabolized by monoamine oxidase (MAO), but with MAO-inhibitors on board, tyramine exerts its effect
Requires Uptake-1 to get into the nerve terminal and inhibits competitively. If Uptake-1 is inhibited by another agent, it cannot exert its effect. |
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Mechanism: 1) Displaces catecholamines out of the nerve terminal, 2) requires Uptake 1 to enter nerve terminal and inhibits End Effect: Increases catecholamines in the synapse Amphetamine Use: Stimulant, drug of abuse (hyperactivity, dilated pupils, dry mouth, erectile dysfunction, tachycardia, increased breathing rate, increased blood pressure, fever, sweating, insomnia, and arrhythmia)
Ephedrine Use: Stimulant, decongestant, appetite suppressant, increase wakefulness |
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Tricyclic Anti-Depressants |
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Mechanism: Inhibits Uptake 1, cross BBB acts on CNS mainly
End Effect: Increases catecholamines in the synapse Use: Depression, SE: sudden death
Note: Examples of TCAs include desipramine, imipramine, amitriptyline |
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Mechanism: CNS: Inhibits Uptake 1, Peripheral: Inhibits Na+ channel End Effect: Increases catecholamines in the synapse; prevents neuronal excitation Use: Local anesthetic, recreational drug (euphoria, increased heart rate, increased blood pressure) |
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decrease BP (pre-synaptic) |
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↑ HR, cardiac contractility |
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Bronchodilation, decrease BP |
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Mechanism: α1, α2, β1, β2 agonist Use: Cardiac arrest, ↑ low cardiac output, anaphylaxis (↓ BP, cardiac output), added to local anesthetics, among other uses
Notes: Action is evenly split between α and β receptor agonism |
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Norepinephrine (Noradrenaline) |
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Mechanism: α1, α2, β1 agonist Use: Hypotension in the critical care setting
Notes: Predominantly stimulates α receptors with relatively little β1 stimulation |
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Mechanism: α1 agonist Use (SE): Decongestant, pupil dilator, septic shock, and profound hypotension |
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Mechanism: α1 agonist Use (SE): Decongestant, pupil dilator, septic shock, and profound hypotension |
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Mechanism: α2 agonist Use (SE): Treatment for hypertension |
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Mechanism: α2 agonist Use (SE): Treatment for hypertension |
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Mechanism: α1, 2 antagonist Use: pheochromocytoma (phenoxybenzamine) |
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Mechanism: α1, 2 antagonist Use: pheochromocytoma (phenoxybenzamine) |
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Mechanism: α1 antagonist Use: Treatment for hypertension |
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Mechanism: α2 antagonist Use: None |
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Mechanism: β1 agonist Use: Stress test, heart failure, shock |
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Mechanism: β2 agonist Use: Asthma, pre-term labor (tocolytic) |
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Mechanism: β2 agonist Use: Asthma, pre-term labor (tocolytic) |
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Mechanism: β1, 2 antagonist Use: Hypertension, migraine prophylaxis |
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Mechanism: β1 antagonist Use: Hypertension, arrhythmia, angina, myocardial infarction |
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Mechanism: β1 antagonist Use: Hypertension, arrhythmia, angina, myocardial infarction |
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Mechanism: α1, β1, 2 antagonist Use: Heart Failure |
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Mechanism: β1 antagonist + vasodilation (NO-like) Use: Hypertension, Heart Failure |
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