Adrenergics Flashcards
Tyramine
- dietary amine usually metabolized by MAO in GI and liver
- in pts w/ MAO inhibitors. tyramine absorbed in large amts. End up with too much tyramine, too much NE being made= Hypertensive crisis
Alpha-methyltyrosine
Inhibits tyrosine hydroxylase (first step in synthesis of catecholamines)
RATE LIMITING STEP
Reserpine
Blocks VMAT (a transporter of bioamines [NE, DA, 5-HT] from cytoplasm into storage vesicles).
- at low doses: leaking of NE into cytoplasm= depletion of NE in neuron (MAO degradation)
- at high doses: overwhelm MAO–> exit into synapticc space through NET, acting in reverse–> transient sympathiomemetic effect
guanethidine
displaces NE in storage vesicles, leading to gradual depletion of NE (if not in storage vesicles, potentially ready to be destroyed by MAO)
amphetamine
displaces endogenous NE (like tyramine)
- weak inhibitor of MAO-
- blocks reuptake by NET and DAT
- little agonist action at alpha and beta receptors, marked behavioral effects
cocaine
potent inhibitor of NET. essentially eliminates catecholamine transport. used as local anesthetic.
imipramine
fluoxetine
inhibitors of NET
tricyclic antidepressants
blocks Na/K ATPase (blocks action potential rom proceeding) and blocks NET
-prevents reuptake of NE and epinephrine=increased DOA
Phenelzine
inhibits MAO-A, increasing NE and 5-HT content
Selegiline
inhibits MAO, increases DA
-low doses for treatment of parkinsons disease
activity of alpha-1 receptor
vasoconstriction, increased peripheral vascular resistance, increase BP, mydriasis, increased closure of internal sphincter of bladder
activity of alpha 2 receptor
feedback receptor. inhibit NE release resulting in decreased BP, inhibit insulin release (pretty much inhibits sympathetics)
activity of B1 receptor
tachycardia, increased myocardial contractility, increased cardiac output, increased renin release, increased lipolysis
activity of B2 receptor
Vasodilation, decreased peripheral vascular resistance, decreased BP, bronchodilation, increased glycogenolysis in liver and muscle, increased glucagon release, relax uterine smooth muscle
direct adrenergic agonists
Epi/NE
- albuterol, pirbuterol, terbutaline
- dobutamine, dopamine
- isoproteranol
- phenylephrine
- clonidine
- salmeterol, formoterol
indirect adrenergic agonists
amphetmine
tyramine
mixed adrenergic agonist
ephedrine
epinephrine
Emergent treatment for asthma, glaucoma. direct- interacts w/ both alpha and beta receptors. (low doses- acts on beta- vasodilation)
(high doses- acts on alpha–vasoconstriction)
CV: 1) B1= (+) ionotropic, chronotropic= increased cardiac output
2) alpha- vasoconstricts arterioles
3) B2= vasodilates vessels to liver and skeletal muscle.
Net result: increased systemic BP
Respiratory: bronchodilation of smooth muscle (b2)
Hyperglycemia: decrease insulin release (alpha2), glycogenolysis increases, increase release of glucagon (b2), lypolysis (b1)
Ephedrine
mixed adrenergic agonist.
ADRs: anxiety, fear, tension, HA, tremor. increase BP, hemorrhage, arrhythmias, pulmonary edema
Interactions: 1) hyperthyroidism- exaggerated CV effects due to increased receptor production. 2) cocaine- exaggerated CV effects due to prevention of reuptake
Norepinephrine
affects alpha1, beta1.
CV: vasoconstriction in periphery= increased BP. baroreceptor reflex: increased BP–> increased vagal activity stimulating baroreceptors causing bradycardia.
Labetolol
Carvediol
Antagonists of A1, B1, B2 receptors.
Causes peripheral vasodilation. doesn’t alter lipid/glucose levels.
Carvediol
Antagonist of A1, B1, B2 receptors.
decreases lipid peroxidation and vascular thickening–benefits CHF
Labetolol
Antagonist of A1, B1, B2 receptors
for HTN, CHF, PIH, HTN emergencies leads to decreased BP
Pindolol
Acebutolol
Antagonists w/ partial agonist activity. (Blocks natural transmitter, but elicits small response itself)
Weakly stimulates B1 and B2 (but unable to respond to more potent catecholamine= decreased cellular effects)
activity: minimize lipid and CHO metabolism.
Used: HTN
