07 Autonomics Flashcards
Autonomic NS anatomical divisions
Sympathetic throacolumbar
Parasympathetic craniosacral
PLANSMA
PANS Long pre-ganglionic fibers Ach Nicotinic Short post-ganglionic fibers Muscarinic Acetylcholine
Preganglionic fibers
Release Ach, receptor: nicotinic
SANS: adrenergic a/b (muscle) muscarinic (sweat glands)
PANS: muscarinic
Somatic NS
Always nicotinic (no ganglia) Receptor: ion channel -> depolarization
Plexuses of ENS
Myenteric (auerbach) = motor activities
Submucosal (meissner) = secretory
Neurotransmitters
Ach = nicotinic and muscarinic
NE = adrenergic
Serotonin (5-HT, ENS)
ANS receptors
Cholinergic: Muscarinic (M1-3) Nicotinic (Nn = nerves, Nm = muscle)
Adrenergic/noradrenergic (A1, A2, B1, B2, B3)
Cholinergic fibers
All preganglionic efferent autonomic fibers
Somatic motor fibers to skeletal muscles
Most PANS postganglionic, some SANS postg
Adrenergic fibers
Most SANS postg
(cholinergic transmission) Synthesis
Choline Acetyltransferase (cytoplasm: acetyl coa [mt] + choline)
Choline transporter: rate limiting step
Inhibitor: Hemicholinium (blocks CHT symporter)
(cholinergic transmission) Storage
VAT: Ach cytoplasm -> vesicles (via proton efflux)
VPG: vesicular proteoglycan bound to vesicular Ach
Inhibitor: Vesamicol (iVAT)
(cholinergic transmission) Release
SNARE proteins
VAMPs (align vesicles): vSNARES close to vesicle (synaptobrevin, synaptotagmin)
SNAPS: t-SNARES close to membrane (syntaxin, SNAP25)
Inhibitor: botulinum toxin (blocks vesicle release)
(cholinergic transmission) Receptor effects correlates
Cholinometrics/cholinergics: direct acting and indirect acting (stimulates PANS)
Anticholinergics: antimuscarinic, antinicotinics (blocks ach receptor)
(cholinergic transmission) Termination of action
AChE: acetate-Ache -> active ache; break down ach, choline is reuptaked
Inhibitors: indirect cholinergics (inhibits ach destruction)
(adrenergic transmission) synthesis
Tyrosine hydroxylase (Tyr -> dopa -> NE/E) Inhibitor: Metyrosine
(adrenergic transmission) storage
VMAT: antiporter on vesicle
Inhibitor: Reserpine (depletes transmitter stores)
(adrenergic transmission) release
Sympathomimetic drugs: release transmitter from vesicles
Inhibitors: Bretylium, Guanethidine (both used for hypertension, G for glaucoma), amphetamine (inhibit MAO)
(adrenergic transmission) receptor effects
Adrenoreceptors: a1, a2, b1/2/3 (targeted by salbutamol and beta blockers), dopamine receptors
Inhibitors: adrenergic receptor agonists and antagonists
(adrenergic transmission) termination of action
Diffusion/reuptake, destroyed by MAO/COMT
NET (uptake 1): carries NE into cytoplasm
Inhibitor: cocaine, tricyclic antidepressants
5HTm
Receptor for locomotion and vasoconstriction
Sumatriptan (for migraine): binds to 5HTm -> vasoconstriction of brain vasculature
Yohimbine (for erectile dysfunction, increasing libido)
5HT3
Stimulates vomiting (5HT3 receptors on vagal afferents & central receptors) Anti-emetics: Ondansetron, metoclopramide (motion sickness)
Integration of CVS function
SANS (increase): peripheral vascular resistance, heart rate, contractile force, venous tone
PANS: decrease HR
Angiotensin II (increase): peripheral vascular resistance, SANS effects
Aldosterone: increase BV
PANS and eye
PANS = constriction of the eye
Organophosphate poisoning = too much constriction
Atropine (anti-cholinergic): PANS inhibitor = blocks eye constriction, cannot be used on pts with glaucoma
Drugs for glaucoma
a-receptor agonism: decrease aqueous production
B-receptor antagonism: inhibits increase of aqueous production
