Adrenergics Flashcards
Heart receptor?
B1
vessel receptor?
A1 = STRONGER = constrict
B2 = dilate (coronary/skeletal)
(a2=little effect)
Kidney receptor?
B1 = release renin
GI tract receptor?
a1 = stop secretion
Sex organs receptor
a1
Uterus receptors?
contract = a1 Relax = b2
Catecholamines
epi
NE
dopamine
NE released at
postganglionic sympathetic
Epi released from
adrenal medulla
Isoproterenol
ISUPREL
selective B ag
Stim the heart
Dopa
CNS transmitter
NE precursor
NE synthesis
Transporter sucks in Tyrosine
Tyr->Dopa->DA->NE->Epi
Inhibit NE release?
- presynaptic a2 receptor
- PGE2
*or degrade w/in terminals w/ MAO; reacumulate from synapse if cleaning
Enhance NE release?
angiotensin II
Most Cirulating Epi broken down by
MAO/COMT
Most of NE removed by
recycled into terminal by NET
receptors effects dependent on
g protein, kinases in target cell
Guanethidine
Mech
enters via NET, depletes NE
Reserpine
Mech
Enters terminal (lipid-solube), stops VMAT, NE can’t be recycled
MAOI inhibitors
Mech
accumulate intracellular NE, increased NE synapse levels
MAOI 8
Rx
Tranylcypromine (anti-depressant)
PARNATE
Amphetamine
Mech
Increase NET activity
more NE release
Faster kinetics than guanethidine/reserpine = gradual NE depletion
Large Tyramine load?
wine, cheese, beer, fava beans
- MAO cleans tyramine, so MAO taken up
- up NE = HTN
- NO MAOIs w/ large tyramine load
Block NET, Up synaptic NE
Rx
Cocaine
Imipramine TOFRANIL
Atomoxetine ASENDIN
Alpha Ag
Phenylephrine
Beta Ag
Isoproterenol ISUPREL
Apha blocker
Phentolamine REGITINE
Beta blocker
Propanolol
Chronic ag treatment causes
desensitization
Downregulation
Chronic blocker treatment causes
supersensitization
Upregulation
NE likes
1s
A1/B1
Isoproteranol likes
Betas
used to stimulate heart
Epi likes
low dose = betas b1 b2
High dose = everything