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45 Cards in this Set

  • Front
  • Back
how can synthesis of Epi, NE or Dopamine be modulated?
inhibit syn at RLS (tyrosine hydroxylase)- not clinically important
incr syn by supplying levodopa (parkinsonism)
false substrates enter syn path at decarboxylation step (b/c non-selective) to form false NTs
what are the 2 primary degradative pathways of NE? where/how does each work?
MAO- neuronal; metab free NE and D in n terminal
COMT- extraneuronal; act in synaptic cleft
what do MAO inhibitors do? COMT inhibitors?
incr NE, D, and 5HT in n terminals in periphery and CNS
COMT inhibitors not used on their own; used with levodopa in parkinsons
where is NE syn?
in vesicles in n terminals
syn from dopamine that enters vesicle via transporter (also moves NE from cytoplasm to vesicle)
what is the action of reserpine?
IRREVERSIBLY INHIBITS transporter on vesicle in n. terminal that moves dopamine in to make NE
result: net loss of NE (also D, 5HT) in n. terminal (degraded by MAO) and decr SNS activity
what are some side effects of reserpine?
PNS dominance:
decr BP
nasal stuffiness
parkinsonism and galactorrhea due to decr D
what is the main method of termination of NE?
reuptake into presynaptic terminals
-neuronal uptake moves NE into cytoplasm
-vesicular uptake moves NE into vesicle
what are 4 subst that block neuronal uptake of NE?
tricyclic antidepressants (imipramine)
antidepressants (SNRIs ex: duloxetine)
adrenergic neuron blockers
what is the effect of cocaine on NE and SNS responses?
responses are potentiated
incr BP and HR
overdose-> MI, CNS bleed
what is the effect of cocaine on adrenergic neuron blockers?
action of adrenergic neuron blockers is impaired by cocaine b/c cant get to site of action
what is the effect of cocaine on indirect sympathomimetic amines?
action is IMPAIRED b/c they cant get to site of action?
what are some examples of drugs that enhance noradrenergic transmission?
amphetamines (incr rel)
cocaine (inhibit reuptake)
phenylephrine (R agonist)
what are ex of drugs that block/reduce noradrenergic transmission?
reserpine (inhibit vesicular storage)
phentolamine (R antagonist)
what is the rank of potencies on aR?
Epi > NE > isoproterenol
what is the rank of potencies on bR?
what antagonist works best on aR?
what antagonist works best on bR?
what are 3 general mxns of actions of agonists?
DIRECT- act on R (NE, Epi)
INDIRECT- incr NE rel (amphetamines, tyramine)
REFLEX effects- if alter BP
what are the CVS effects of NE?
activates a1,a2, b1
incr TPR
direct incr in HR
reflex decr in HR
what are the CVS effects of Epi?
activates a1, a2, b1, b2
at low doses has b2 affects- vasodilation
at high doses has a1 affects- vasoconstriction
incr in HR (b1)
systolic BP incr but diastolic BP may go down
what are the CVS effects of isoproterenol?
acts on b1, b2
lg incr in HR (direct and reflex)
overall decr in TPR; early incr in systolic BP due to incr in contractility
what are 3 types of mm with b2R?
bronchial sm m
vessel sm m
uterine sm m
how does the b2R mediate sm m relaxation?
incr cAMP via Gs
also incr glycogenolysis
which receptors are mediated by an incr in IP3/DAG?
a1 (Gq)
which receptors act via an incr in cAMP?
b1, b2, b3, D1
which receptors act via a decr in cAMP?
a pt that has taken cocaine presents with incr HR and BP. what mxm mediated the incr in HR?
incr cAMP via b1R
a pt on phenylephrine for nasal congestion presents with in incr in BP. what mxn underlies the incr in BP?
incr IP3, DAG via a1
what are the effects of a1R activation?
mydriasis due to contraction of the dilator mm of the pupil
what are the effects of a2R activation?
inhibits adrenergic and cholinergic n terminal rel
inhibits insulin rel from pancreatic beta cells
some vasoconstriction
what are the effects of activation of b1R?
incr rate and contractility of heart
incr conduction velocity
stim renin rel from JG cells
what are the effect of activation of b2R?
bronchial, vascular and uterine sm m relaxation
TREMOR (somatic n terminals)
stim glycogenolysis in liver
what is the importance of the b3R?
inhibits contraction of detrusor m
involved in lipolysis
what are the terms for incr HR, incr contractility and incr conduction velocity?
positive chronotropism, inotropism, dromotropism
is NE or Epi a potent bronchodilator?
mediated by b2R
also decr mast cell secretion
what are the effects of dobutamine?
activate b1R
no change in TPR
direct incr in HR, no reflex
what R does phenylephrine act on?
a1>a2 agonist
what R does clonidine act on?
a2>a1 agonist
what R does isoproterenol act on?
b1=b2 agonist
what does terbutaline do? what are some ex of other drugs in the same catergory?
b2R agonist
also salmeterol (long acting)
albuterol, metaproterenol (short acting)
what are 3 important uses of a sympathomimetics?
1. reduce regional blood flow: local anesthetics in dentist, prolongs local effect and slows systemic absorption
2. nasal decongestants: if taken systemically may cause incr BP, can only use 4-5d or become habituated; ex: phenylephrine, oxymetazoline
3. dilate pupil
why is NE not used in conjunction with local anesthetics?
causes too much vasoconstriction because has no b2R effect
may cause sever ischemia and sloughing of tissues
what is an ex of an a1-sympathomimetic?
specific a1R agonist
incr TPR-> incr BP-> reflex bradycardia
can block reflex bradycardia with atropine (muscarinic antagonist)
used clinically for: hypotensive states
nasal decongestion
what is an ex of an a2 agonist?
decr SNS outflow
used for HTN or opiod withdrawal
what is an ex of a b1 agonist?
used for short term management of pump failure (after surgery, MI, acute CHF)
long term efficacy uncertain: enhance renal perfusion despite low CO