SYMPATHOMIMETIC DRUGS Flashcards
Natural Catecholamines what are they called? what are 3 examples?
endogenous
EPI
NE
Dopamine
Synthetic catecholamine
2
Isoproterenol
Dobutamine
Synthetic non-catecholamine (Indirect acting)
4
Ephedrine
Mephentermine
Amphetamine
Metaraminol
Synthetic non-catecholamine (Direct acting)
2
Phenylephrine
Methoxamine
what medication inhibits the transport of dopamine into the synaptic vesicle
reserpine
what does dopamine become when it enters the vesicle
norepinephrine
which 2 drugs blocks the release of NE from the presynaptic cell membrane
guanethidine and bretylium
how is NE released from the cell membrane
exocytosis from the Ca++ influx
once NE is released it binds to the receptors activating what
adenylate cyclase
once NE activates adenylate cyclase what does it do next
opening of ion channel/ formation of cAMP
once NE channels are open and camp is activated what is the last step
contraction of arterial smooth muscles, increase heart rate and contractility
removal of NE. what inhibits reuptake
cocaine and TCA
what metabolizes NE
COMT (PLASMA) and MAO (synaptic cleft)
what are Adrenergic Receptors
a1, a2, b1, b2, b3
what are cholinergic receptors
nicotinic and muscarinic receptors
a1 Receptors
located where?
vascular smooth muscle of skin
splanchnic regions
GIT
bladder sphincter
radial muscle of iris
a1 Receptors what is their effect?
Produce excitation (contraction of vascular smooth muscles)
a1 Receptors what are they equally sensitive to?
NE and EPi
a1 receptor arterial vasoconstriction leads to what CV effects ?
increase SVR, LV afterload, and BP
a1 receptor venous vasoconstriction causes what effect ?
increase venous return, increase SV, increase CO
a1 receptor stimulation inhibit what
insulin secretion and lipolysis
a1 receptor m/a
formation of IP3 and increased intracellular calcium
a1 receptor pre synaptic or post synaptic?
postsynaptic adrenergic
a2 receptors location?
presynaptic membrane & postsynaptic in brainstem, walls of GIT, platelets, and fat cells
a2 receptors are postsynaptic in?
brainstem, platelets, fat cells, and walls of GIT
a2 receptors produce
inhibition of NE release and synthesis (relaxation and dilatation) blocks Ca entry
a2 receptors produce what type of feed back loop
-ve
a2 receptors inhibit what
sympathetic outflow in brain stem
a2 receptors produce
sedation and analgesia in substantia gelatinosa
a2 receptors m/a
inhibition of adenylate cyclase, decrease camp and decreases ca entry
b1 receptors are located where
sa node and av node ventricular muscle
b1 receptors produce
excitation, increase hr, increase conduction, increase contractility, and increase cardiac output.
b1 receptors are sensitive to
NE and EPI
b1 receptors m/a
activation of adenylate cyclase and increase camp
b2 receptors location
smooth muscle of skeletal muscle blood vessel
bronchial smooth muscle
walls of GIT and bladder
b2 receptors produce what?
relaxation (dilation of vascular smooth muscle, dilation of bronchioles, relaxation of the pregnant uterus- tocolysis)
b2 receptors also produce increase
bg calorigenesis
glycogenolysis and gluconeogenesis
b2 receptors m/a
activation of adenylate cyclase and increase cAMP (same as b1)
b3 receptors located where
gallbladder and adipose tissue
b3 receptor function
unknown function
nicotinic receptors located where
autonomic ganglia (Nn) of the sympathetic and parasympathetic neuromuscular junction(n1) and adrenal medulla (n2) the receptors at these locations are similar but no identical
nicotinic receptors are activated by
ach or nicotine
nicotinic receptors produce
excitation
cholinergic receptors nicotinic receptors ganglion blockers examples and what do they do
hexamthonium trimethaphan block the nicotinic receptors for Ach in autonomic ganglia but not at the NMH
cholinergic receptors nicotinic receptors m/a
opening of Na+ and K+ channels
cholinergic muscarinic receptors - location
in heart (m2) smooth muscle (m3) (except vascular smooth muscle) and glands(m3)
cholinergic receptors muscarinic receptors -activated by
Ach and muscarine
cholinergic receptors muscarinic receptors are inhibitory
in heart (decrease heart rate decrease conduction velocity in AV node)
cholinergic receptors muscarinic receptors are excitatory
in smooth muscle and glands increase motility and increase secretion
cholinergic receptors muscarinic receptors are blocked by
atropine
cholinergic receptors muscarinic receptors mediate
sux induced bradycardia
cholinergic receptors muscarinic receptors m/a
in heart?
in smooth muscles?
in heart sa node: inhibition of adenylate cyclase leads to opening k channels, slowing rate of phase 4 depolarization and decrease heart rate.
in smooth muscles and glands: formation of IP3 and increase intracellular Ca++
cAMP Mechanism receptors
B1 &B2 & A2
receptors couples with ion channels
cholinergic nicotinic
IP3 mechanism receptor
A1 receptor
cholinergic muscarinic
Nitric Oxide utilizes this second messanger
cGMP
Epinephrine
mechanism
application
Direct general agonist (a1, a2, b1, b2)
Anaphylaxis, glaucoma (open angle) asthma, hypotension with LA
Norepinephrine
mechanism
application
a1, a2, b1
hypotension decrease renal perfusion organ ischemia
isoproterenol
mechanism
application
B1=B2
av block (rare)
dopamine
mechanism
application
D1=D2 >b>a
shock increase renal perfusion and GFR heart failure
dobutamine
mechanism
application
b1>b2
shock and CHF
amphetamine
mechanism
application
indirect general agonist
releases stored catecholamines
narcolepsy, obesity, adhd
ephedrine
mechanism
application
indirect general agonist, releases stored catecholamines
nasal decongestants urinary incontinence hypotension hypotension with epidural/spinal anesthesia
phenylephrine
mechanism
application
a1>a2
pure a agonist
pupil dilation vasoconstrictor increase SVR increase MAP nasal decongestant
albuterol, terbutaline
B2>b1
asthma & premature labor
cocaine
mechanism
application
indirect general agonist uptake inhibitor
causes vasoconstriction and local anesthesia
clonidine & a-methyl dopa
centrally acting a2 agonist, decrease central sympathetic outflow
hypertension, decrease MAC, increase Anesthesia/analgesia
Nonselective Beta 1 Beta 2 antagonist (propranolol) what effect ok K+ level?
Hypokalemia prevention .
( explanation) By blocking beta 2 .Prevents the Beta 2 activation of Na/K pump which causes K+ to move inside inside cell. Prevent the K movement inside cell, prevents hypokalemia.
Cardioselfrive Beta 1 antagonist ( atenolol ) effect of K+level
Cause hypokalemia
