Adrenergic agonists Flashcards
adrenergic receptor agonists are – drugs
sympathomimetic
what type of receptor are adrenergic receptors?
G-protein coupled
adrenergic receptor’s structure
7 transmembrane segments
dopamine as a – also activates adrenergic receptors
catecholamine
catecholamines are monoamines, organic compounds that have a – (benzene with two hydroxyl side groups) and a side chain amine
catechol
example of a synthetic catecholamine
levonordefrin
only catecholamine that doesn’t discriminate between adrenoreceptor subtypes
EPI
catecholamines are released from –
postganglionic sympathetic terminal and adrenal glands
after its release, catecholamines act on –
postsynaptic receptors or directly into circulation
albuterol
direct acting noncatecholamine
receptors for albuterol
beta 2
clonidine
direct acting noncatecholamine
phenylephrine
direct acting noncatecholaimine
receptors for clonidine
alpha 2
receptors for phenylphrine
alpha 1
function of indirect acting noncatecholamine
cause NE release or blocks reuptake
alpha and beta 1
NE and tyramine and amphetamine
tyramine
indirect acting noncatecholamine
receptors for tyramine
alpha and beta 1
receptors for amphetamine
alpha (CNS) and beta 1
mixed acting noncatecholamine
ephedrine
receptors for ephedrine
alpha (CNS), beta, NE release
not effective orally
catecholamine
no direct effects on CNS
catecholamine
short acting
catecholamine
many are effective orally
noncatecholamine
many have effects on CNS
noncatecholamine
many are longer acting
noncatecholamine
many are more selective in action
noncatecholamine
chemical properties of catecholamines
polar and aqueously soluble
receptors for isoproterenol
beta 1, beta 2
receptors for dobutamine
beta 1
receptors for levonordefrin
alpha 2, beta 1
– receptors are close to sites of NE release from postganglionic neuron vasicosities
alpha 1
exogenously administered sympathomimetics or EPI/NE released from adrenal glands will affect the post junctional – receptors that sit outside the varicosities
alpha 2
catecholamines are not effective orally because they are – and will dissolve in water
polar compounds
catecholamines are not effective orally because they are inactivated by –
digestive enzymes
if catecholamines are given – or gingival retraction cord catecholamine, (if not broken down by enzymes) will be rapidly absorbed by the oral tissues and induce their effects
sublingually
why do catecholamines have no direct central effects?
polar so they can’t cross blood brain barrier
why are catecholamines short acting?
efficient reuptake; metabolic breakdown
why are non-catecholamines effective orally?
non-polar
why are non-catecholamines effective in CNS?
can cross blood brain barrierf
serotonin and NE reuptake inhibitor antidepressants exhibit exaggerated response at –
synaptic clefts
serotonin and NE reuptake inhibitor antidepressants lead to –
greater amounts of NE in synapse = happiness
tricyclics
antidepressant
what are tricyclics used for?
pain management
selective serotonin reuptake inhibitors
antidepressant
serotonin-NE reuptake inhibitors
antidepressant
what are serotonin-NE reuptake inhibitors used for?
pain management
monoamine oxidase inhibitors
antidepressant
trazadone and remeron are antidepressant used for –
sleep aides
two marketed drugs that are COMT inhibitors
entacapone and tolcapone
function of COMT inhibitors in Parkinson patients?
prevent l-Dopa metabolism to dopamine (as well as inhibit EPI/levonordefrin metabolism)
