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25 Cards in this Set

  • Front
  • Back
alpha 1 receptors?
which chem?
constrict blood vessels of skin, mucosa, kidneys

Epi, NOREP, not really Isopret
alpha 2 receptors?
which chem?
unique mechanism of action?
Pre synaptic terminal
INHIB Auto receptor
NOREP/EPI have different sensitivities
decrease cAMP
B1 receptors?
increase HR, contractility, rate of conduction
increases cAMP
B2 receptors?
clinical use?
dilation of smooth muscle
asthma attacks (bronchial smooth muscle)
ISO>EPI but NOREP is useless
Remember, EPI Pen for rxn
increase cAMP
symp pre? post? 3 combos
1. Ach, Norep for smooth muscle, cardiac, and gland secretions

2. ACh, ACh for sweat glands
3. ACh (adrenal medulla), EPI/NOREP for reg of carb and fat metabolism
parasym pre? post? what specific receptor type?
ACh, ACh, MUSCARINIC (g coupled) for smooth, cardiac, glands
Epi effect on CV system?
increase HR B1
dilate smooth muscles (decrease peripheral resistance, BP)
NET: slight increase in HR
NROEP Effect on CV system?
increase HR B1
constriction of skin, mucosa (increase BP and peripher resistance) A1
NET: strong vagal response and decrease HR due to increase BP
ISO effect of CV sys?
increase HR B1
dilation of smooth muscles B2 (decrease BP)
NET: strong increase in HR due to vagal response plus B1 effect
enyzmes that breakdown catecholamines?
MAOI, then COMT, aldehyde reductase, and aldehyde dehydrogenase
what does reserpine do?
blocks the uptake of catecholamines into interneuronal stores
Uptake 1?
Uptake 2?
1. reuptake of NOREP into nerve endings; HIGH affinity, LOW capacity
2. reuptake in extraneuronal env; LOW affinity, HIGH capacity
cocaine's effect on catecholamine reuptake?
blocks NE/EPI reuptake in nerve terminals, resulting in CNS stimulation
Direct vs. Indirect acting sympathomimetic Amines?
what if taken with reserpine?
direct- agents act right on receptors
indirect- displace NOREP from nerve terminals from vesicles
** can't work if reserpine blocks reuptake
Effect of amine structure?
# of OHs?
more OH's, the inceased affinity for storage and the decreased bioavailabilty

more polar, less bioavailability and won't be able to cross BBB
False Transmitter Concept? (role of exogenous amines)
exogenous amines are taken up at nerve terminals, causing the release of EPI/NOREP and leading to a response
Beer, Cheese and WINE Rule?
MAOI interactions?
if taking MAOIs (which increase NOREP way more than normal), metabolism of tyramine leads to greater displacement and you get major CNS stimulation
Side Effects of sympathetic Antagonists? (4)...think alpha 1 antagonists
Orthostatic (postural) HYPOTensions
Increase GI motility
sexual side effects
ACh production in nerve terminals? what key enzyme and what is necessary to complete?
actelytransferase and must have choline receptors to bring it into terminal
all have what common effect?
blocks choline entry
blocks ACh synaptic receptor
prevents ACh release from synaptic vessicles
mechanism for Nicotinic AChRs?
where found?
ligand gated
always at NMJs
AChE Inhibtors? what type of variation? How about organophosphates?
short/long term acting, permanent/irreversible activity with organophosphates
muscarinic AChr's?
M1- what result and molecular mechanism?
M2- what result and molecular mechanism?
M1= odd- 1,3,5 EXCITATION via PLC and PKC
M2= even 2,4 INHIBITION via decrease adenyl cyclase (cAMP)
Succinylcholine? used for what? what type of AChR does it act on?
Scopollamine (airplane)? what type of AChR? action?
acts on nicotinic and it causes reversible paralysis at NMJ- used as anesthetic

peripheral/central antagonist of muscarinic ACHRs
crosses BBB and used prophalyactically for motion sickness
What occurs with atropine poisoning? i.e is it a para or symp agonist or antagonist?
too much peripheral anatagonist *** knock out parasymp***
dry mouth, tachycardia, dilated pupils etc, (SYMP signs)