Adrenergic stimulants general info Flashcards
tyrosine is _____ to become l dopa
hydroxylated
l dopa is ______ to dopamine
decarboxylated
DA is _______ to form NE in noradrenergic neurons synaptic vesicles
hydroxylated
rate limiting pathway of DA/NE/Epi production
conversion of tyrosine to l dopa (hydroxylation which occurs in cytoplasm of presynaptic knob)
NE is converted to epi in the
adrenal medulla
drugs that cause release of NE from the presynaptic terminal
tyramine
amphetamine
only have effect if the noradrenergic innervation is intact
a patient comes in with severe denervation and you want to provide them with sympathetic stimulation. what class of drugs aren’t going to work?
indirect adrenergic stimulants
action of NE is terminated by
reuptake
drugs which block NE reuptake
cocaine, antidepressants
MAO hangs out _________ and breaks down NE that’s _______
outer surface of mitochondria
released in the presynaptic terminal
MAO
monamine oxidase
COMT
catechol O methyl transferase
measure these in 24 hour urine to evaluate NE/Epi metabolism
VMA and HVA
VMA
3 methoxy 4 hydroxy mandelic aci
HVA
homovanillic acid
relaxation of blood vessels supplying skeletal muscle
B2
relaxation of smooth muscle in gut and bronchial tree
B2
increase rate and contractility of the heart
B1 B2
increase glycogenolysis in liver/muscle, lipolysis from adipose cells
B2 B3
3 indirect adrenergic stimulant MOAs
- increase release of NE from nerve endings
- inhibit reuptake of NE
- inhibit metabolism of NE
depletion of NE stores would mean that
indirect adrenergic stimulants can’t work
denervation has _________ on direct acting adrenergic stimulants
no effect or enhances effect (receptors are up regulated, super sensitive)
contraction of the prostate gland
a1
stimulate pilomotor smooth muscle causing erection of hair
a1
Cause aggregation of platelets
a2
Decrease insulin secretions
a2
Contract some vascular smooth muscle
a2
neurotransmitters on B1 receptors
NE=epi
isoproterenol has a high affinity for
all beta receptors
neurotransmitters on B2 receptors
Epi!!!!!!!! high affinity
NE has little effect
increase secretion of renin from the kidney
B1
promote potassium uptake into skeletal muscle
B2
D2 receptors
Inhibit adenylyl cyclase, open potassium channels, decrease Ca++ influx
dilates renal blood vessels
D1
receptor that inhibits release of transmitters from nerve terminals
D2
alpha receptor effect on veins
contracts reservoir veins increasing filling pressure of the heart
reduce venous capacity
vessels that are more densely innervated and therefore alpha stimulation has the largest effect on them
small vessels
why does alpha stimulation cause slowed heart rate
increases blood pressure causes baroreceptor reflex to slow heart by vagal input
impaired baroreceptor response —> increased sensitivity of blood pressure to alpha agonists
atherosclerosis
glaucoma tx: increase removal of aqueous humor decreasing intraocular pressure
alpha receptor agonists
decrease diastolic blood pressure
B2 (dilation of blood vessels in skeletal muscle)
increases automaticity by increasing conduction velocity
beta receptor stimulation
increases coronary blood flow
beta receptor stimulation
increased rate, contractility of heart
beta receptor stimulation (may be countered some by reflex bradycardia)
glaucoma tx: block increased production of aqueous humor by
blocking beta receptors (beta receptor antagonists)
asthma treatment
B2 receptors
treat premature contractions in pregnancy
relax the uterus with a B2 agonist
your patient is hyperglycemic, what med might they be taking?
B2 agonist –> glycogenolysis in the liver
your patient is hypokalemic, what medication might they be taking?
B2 agonist –> increased uptake of K+ into cells
insulin secretion (a lil bit) stimulated by
B2 receptors