09 - Adrenergic Pharmacology Flashcards
Norepinephrine
primary transmitter at the sympathetic postganglionic neuron effector cell synapses in most tissues
exceptions:
- eccrine sweat glands
- vasodilator sympathetic fibers in skeletal muscle
Dopamine/Norepinephrine on renal blood vessels
dopamine vasodilates renal blood vessels
norepinephrine vasoconstricts
Tyrosine is hydroxylated by tyrosine hydroxylase to
DOPA
Tyrosine hydroxylase is inhibited by
metyrosine
DOPA is decarboxylated to
dopamine
dopamine is hydroxylated to
norepinephrine
NE and dopamine are transported into vesicles
inactivated by:
monoamine oxidase in the cytoplasm
increase stores of NE and dopamine
MAOIs
vesicular transport inhibted by
reserpine
entry of calcium triggers interaction among
SNARE proteins (VAMPs and SNAPs)
What are SNARE proteins
“SNAP (Soluble NSF Attachment Protein) REceptor”
The primary role of SNARE proteins is to mediate vesicle fusion, that is, the fusion of vesicles with their target membrane bound compartments (such as a lysosome). The best studied SNAREs are those that mediate docking of synaptic vesicles with the presynaptic membrane in neurons. These SNAREs are the targets of the bacterial neurotoxins responsible for botulism and tetanus.
entry of calcium inhibited by
promoted by
guanethidine
amphetamines and tyramine
diffusion and reupate via NET and DAT in synaptic cleft
inhibited by
cocaine and TCAs
metabolized by MAO and COMT into
inhibited by
metanephrines and VMA
MAOIs and COMT inhibitors (duh)
Site of autonomic drug action:
synthesis cholinergic and adrenergic inhibitors
hemicholinium
metyrosine
Site of autonomic drug action:
storage cholinergic and adrenergic inhibitors
vesamicol
reserpine
Site of autonomic drug action:
release cholinergic and adrenergic inhibitors
botulinium
guanethedine
Site of autonomic drug action:
termination metabolism cholinergic and adrenergic inhibitors
neostigmine
MAOIs, COMTIs
Site of autonomic drug action:
termination reuptake cholinergic and adrenergic inhibitors
none
cocaine, TCAs
drug effects on adrenergic transmission
used in treatment of several diseases (pheochromocytoma, hypertension)
block sympathetic but NOT parasympathetic functions
other drugs promote catecholamine release - predictably cause sympathomimetics effects
a1 adrenergic effects
- most vascular smooth muscle
contracts (increased vascular resistance)
a1 adrenergic effects
- pupillary dilator muscle
contracts (mydriasis)
a1 adrenergic effects
- pilomotor smooth muscle
contracts (erects hair)
a1 adrenergic effects
- liver (in some species, eg, rat)
stimulates glycogenolysis
a2 adrenergic effects
- adrenergic and cholinergic nerve terminals
inhibits transmitter release
a2 adrenergic effects
- platelets
stimulates aggregation
a2 adrenergic effects
- some vascular smooth muscle
contracts
a2 adrenergic effects
- fat cells
inhibits lypolysis
a2 adrenergic effects
- pancreatic B cells
inhibits insulin release
B1 adrenergic effects
- heart
stimulates rate and force
B1 adrenergic effects
- juxtaglomerular cells of kidney
stimulates renin release
B2 adrenergic effects
- airways, uterine, and vascular smooth muscle
relaxes
B2 adrenergic effects
- liver (human)
stimulates glycogenolysis
B2 adrenergic effects
- pancreatic B cells
stimulates insulin release
B2 adrenergic effects
- somatic motor neuron terminals (voluntary muscle)
causes tremor
B2 adrenergic effects
- heart
stimulates rate and force
B3 adrenergic effects
- fat cells
stimulates lipolysis
dopamine1 (d1) adrenergic effects
- renal and other splanchnic blood vessels
dilates (decrease resistance)
d2 adrenergic effects
- nerve terminals
inhibits adenylyl cyclase
beta receptors mnemonic
1 heart, 2 lungs
b1 heart
b2 lungs
