Autonomic Pharmacology Flashcards
Nicotinic receptors
occasionally targeted for a non-elective effect bc it affects both the SNS and PSNS
NT synthesis
tyrosine –> dopa –> dopamine –> NE –> epinephrine
M1, M3, M5 receptor
Tend to cause contraction (stimulatory)
- M3 in bladder wall: contracts
- M3 in sphincter: relaxes
(GI tract too)
M2, M4 receptors
Tend to be inhibitory
M2: decrease heart rate, decrease contraction
M2: bronchoconstriction
Stimulating M receptors
Direct: agonist
Indirect: acetylcholinesterase inhibitor (reversible vs irreversible)
- acetylation
- carbamylation
- phosphorylation
Parasympatholytics
aka anticholinergics or antimuscarinics
- block PSNS responses
ex. ATROPINE
Atropine Uses
- intubation
- ophthalmology
- asthma
- antidote
alpha 1 receptor
constriction of smooth muscles
- sphincters
- blood vessels (vasoconstriction)
alpha 2 receptor
inhibition of presynaptic NE release
beta 1 receptor
stimulates the heart
- increased heart rate
- atrioventricular conduction
- increased contractility
kidney
- stimulate the release of RENIN (causes increase in blood pressure)
beta 2 receptor
relaxation of smooth muscles
- lungs (bronchodilation)
- blood vessels in skeletal muscle (vasodilation)
- GI tract, bladder, uterus
liver
- mediate glucose release by gluconeogenesis or glycogenolysis
Sympathomimetics
- directly activate adrenergic receptors (NE, adrenaline)
- increase amount of sympathetic neurotransmitter in synapse
- release
- reuptake
- metabolism (MAO: monoamine oxidase) –> MAO inhibitors
Sympatholytics
- directly block receptors
ex. propanolol - decrease amount of sympathetic neurotransmitter released
ex. clonidine
(alpha 2 agonists)
Iris muscle (circular, sphincter)
M2, M3 receptors
*note M2,M3 also contracts ciliary muscle (controls the lens) –> opens trabecular meshwork and canal of schlemm for treatment of glaucoma
- too much stimulation causes lens to bulge
radial muscle (longitudinal)
alpha 1 receptors (dilation)