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what happens with chronic exposure of agonist? of antagonist?
- agonist = down regulation
- antagonist= up regulation
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on postsynaptic a1 receptor?
vasoconstriction, mydriasis, increase HR contractility, increase sphincter contractility (GI, bladder), relax GI, decrease insulin release
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on presynaptic a2 receptor?
- DECREASE SYMPATHETIC OUTFLOW
- DECREASE INSULIN RELEASE
- DECREASE LIPOLYSIS
- DECREASE NE RELEASE FROM POSTSYNAPTIC MEMBRANES i.e clonidine, precedex
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postsynaptic a2 receptors?
- platelet aggregation
- CNS hyperpolarization
-
postsynaptic B1 receptor?
- increase Heart contractility
- increase HR
-
postsynaptic B2 receptor
- VASODILATION, BRONCHODILATION, STIMULATES INSULIN RELEASE,
- GI RELAXATION, UTERIN RELAXATION, BLADDERRELAXATION, GLYCOGENOLYSIS, LIPOLYSIS, STIMULATION OF SODIUM/POTASSIUM PUMP
-
Dopa 1 receptor
- RENAL VASODILATION
- MESENTERIC VASODILATION
-
dopa 2 receptor?
decrease sympathetic outflow
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describe adrenergic transmission of tyrosine to NE?
- 1.Tyrosine enters terminal dendrite
- 2.Tyrosine is converted into dopamine
- 3.Via ATP, dopamine gets vesicle around*(reserpine blocks it)
- 4.Dopamine is converted to NE
- 5.Ca+ carries vesicle to wall
- 6.NE released into synapse
- 7.NE:Reaches postsynaptic cleft and contacts α1α2β1β2
- Is metabolized in synapse by “MAO” into dopamine or tyrosine( gets reused)
- Reaches presynapticcleft α2 ONLY (acts as an autoreceptorfor autonomic NS)
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what are the steps in cholinergic transmission?
- 1.Choline enters terminal dendrite
- 2.Cholinejoins acetyl-coenzyme A and forms ACh
- 3.Via ATP, ACh gets vesicle around it
- 4.Ca+ comes into terminal dendrite and carries vesicle to wall
- 5.ACh released into synapse
- 6.ACh:a)Reaches postsynaptic cleft and contacts nicotinic or muscarinic receptor
- b)Is metabolized by acetylcholinesterase
- i. choline is reused (it is the presynaptic reuptake of choline that is main regulator of ACH)
- ii. Acetate is waste product
- c)Reaches synaptic cleft then contact autoreceptors that tell axon to stop producing ACh because of accumulation
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what are nicotinic receptors stimulated by? blocked by?
- stimulated by nicotine, ACH, Mech, DMPP
- blocked by Hexa and decathmethomium d tubbocurare
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what are the 2 types of nicotinic recpetors? what are they stimulated by? blocked by?
- Ganglionic is stimulated by Nictoine, ACH, DMPP and blocked by Hexamethonium and d tubocurare
- Neuromuscular is stimulated by Nicotine, ACH
- blocked by decamethonium and atropine
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what stimulated muscarinic receptors? blocks them?
- stimulated by muscarine, ACH, CCH, MEch,
- blocked by atropine, scopolamine
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what blocks the muscarinic receptors?
blocked by atropine, dicyclomine, pirezepine, gallamine, HHSD
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