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Flashcards in Autonomic Nervous System Deck (48)
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3 sympathetic nervous system activations

all positive effects via beta1-adrenergic receptors (usually norepinephrine)
-stimulate heart via SA node
-stimulate AV nodal condunction
-stimulate myocardial (ventricular) contractility


3 parasympathetic nervous system activations

all negative effects via muscarinic cholinergic receptors (usually ACh)
-inhibit heart rate at SA node
-inhibit AV nodal conduction
-inhibit atrial contractility (mild compared to sympathetic ventricular stimulation)


sympathetic VS parasympathetic in regards to preganglionic VS postganglionic fibers

symp: pre are short, post are long
para: pre are long, post are short and close to target tissues


locations of pre VS postganglionic fibers

pre: lie in CNS in columns in brain stem and spinal cord; exit to make synapses
post: in peripheral ganglia that project to target tissues


A, B, and C fibers

A: large-diameter, fast conducting myelinated motor neurons of skeletal muscle
B: small diameter, slow conducting myelinated preganglionic axons
C: small diameter, slow conducting unmyelinated postganglionic axons


divergence in SNS VS PNS

SNS: one preganglionic axon can contact ~100 postganglionic neurons by collateral branching
PNS: one preganglionic axon contacts 15-20 postganglionic
-enables widespread responses to numerous effectors when necessary


varicosities (in passing synapses)

characteristic of autonomic nervous system, with single axon having broad actions in target tissues


somatic nervous system origin, ganglia, and target organs

central nervous system, w/o ganglia, to skeletal muscle
-N1 nicotinic acetylcholine receptor on muscle


parasympathetic axon system origin, ganglia, and target organ

autonomic nervous system, w/ ganglia, to smooth muscle, cardiac muscle, or glands
-ganglion has N2 nicotinic cholinergic (ACh) receptor
-release ACh to muscarinic ACh receptor on organ (M1-5)


sympathetic axon system origin, ganglia, and target organ

autonomic nervous system, w/ ganglia, to smooth muscle, cardiac muscle, and glands, including adrenal glands
-ganglion has N2 nicotinic cholinergic (ACh) receptors
-all except adrenals and sweat have alpha/beta-adrenergic receptors (NE>E)
-adrenal "ganglion" Chromaffin cell has N2 receptor for ACh, and releases E to alpha/beta adrenergic receptors all over body
-sweat glands have mjuscarinic ACh receptors


Chromaffin cells

in adrenal medulla, and directly innervated by SNS
-release mostly epinephrine (80%), and carried in body to various tissues
-last 5-10 times longer b/c inactivated slowly, and reach tissues not innervated by sympathetic


mechanism of action of alpha1-adrenoreceptors (active VS inactive); GPCR metabotropic

inactive: alpha-q subunit of Gq is bound to GDP
active: NE bound to receptor, so alpha-q bound to GTP
-active to phospholipase C, which releases PIP2 that breaks into DAG and IP3
-IP3 releases Ca++, which acts on PRO kinase C with DAG


mechanism of action of beta-adrenoreceptors (active VS inactive); GPCR metabotropic

inactive: alpha-s subunit of Gs is bound to GDP
active: NE bound to receptor, so alpha-s bound to GTP
-active to adenylyl cyclase, which converts ATP to cAMP


mechanism of nicotonic cholinergic receptors; odds VS evens; GPCR metabotropic

M1, 3, 5: PLC leads to generation of IP3 and DAG (like alpha1 adrenergic receptors)
M2, 4: inhibition of adenylate cyclase causes decreased cAMP (opposite of B1/2)


antagonists of
N1 (nicotinic ACh)
N2 (nicotinic ACh)
M1/3/5 (muscarinic ACh)
M2/4 (muscarnic ACh)
beta1 (adrenergic)

N1 - d-Tubocuraine
N2 - hexa-methonium
M1-5 - atropine (less selective for 2/4)
beta1 - propranolol


alpha 1 metabotropic adrenoreceptor effects in SNS

mydriasis (pupil dilation) and eyelid retraction
sphincter contraction
alpha+beta: epinephrine from adrenal medulla, smooth muscle wall contraction


beta metatropic adrenoreceptor effects in SNS

1: increased heart rate and force of contraction
2: bronchial dilation
alpha+beta: epinephrine from adrenal medulla, smooth muscle wall contraction


muscarinic cholinergic metatropic effects on SNS



epinephrine VS norepinephrine targets

E: beta-adrenergic receptors (CO, BMR, bronchiodilation, inhibit intestines)
NE: alpha-adrenergic receptors (BP elevation, urinary excretion)


pheochromocytoma cause, effect, treatment

tumor of the adrenal medulla (rarely extramedullary sites) secretes excessive amounts of NE, and less so E (since not enough cortisol); rarely increase dopamine
-sustained (rarely episodic) HTN
-in all ages/genders, esp. 40-50 yrs
-treat by excising well-circumscribed tumors (1 gram to kilograms)
-treat symptoms with alpha1 and beta1-adrenergic antagonists


Horner syndrome effects, types of lesions

injuries to SNS make ipsilateral lesions causing miosis (constricted pupil), ptosis (drooping eyelid), anhydrosis (lack of sweating)
-1st order lesion: brainstem interrupting descending tracts (stroke)
-2nd order lesion: preganglionic sympathetic cell bodies or fibers supplying eye synapse in superior cervical ganglion
-3rd order lesion: postganglionic sympathetic cell bodies or fibers


pupillary constriction/miosis is controlled by?

CN III (pupillary light reflex); occulomotor


gland secretion is controlled by?

CN VII - nasal/lacrimal/submandibular
CN IX - parotid (glossopharyngeal)
CN X - gastric, pancreatic


GI peristalsis is controlled by?

CN X - increased motility and sphincter relaxation


bronchial constriction and decreased heart rate is controlled by?

CN X (heart is beta1 receptors; chonotropic and inotropic; lung is beta2 receptors)


what does a cardiac vagotomy do?

cut the vagus nerve
-increases heart rate to 160 bpm, and compensatory mechanisms take many months to restore HR to normal


where does the vagus nerve originate?

from dorsal motor nucleus of vagal nerve in the medulla


what controls more than 75% of the PNS?

the 2 vagal nerves


what are supraspinal nuclei containing neurons part of?

the ANS; contain cell bodies of pregnanglionic parasympathetic neurons (efferent)


Edinger-Westphal nucleus

contains cell bodies of preganglionic parasympathetic fibers that travel with CN III to ciliary ganglion


superior salivatory nucleus

contains cell bodies of preganglionic fibers that travel with CN VII to pterygopalatine and submandibular ganglia


inferior salivatory nucleus

contains cell bodies of preganglionic fibers that travel with CN IX to otic ganglion


nucleus ambiguus (rostral portion and the rest)

rostral: contains preganglionic cell bodies that distribute with CN IX
the rest: along with dorsal motor nucleus of vagus, contains cell bodies of preganglionic fibers that travel with CN X to host of terminal ganglia in viscera of thorax and abdomen


nucleus trachus soltarius (NTS)

not part of the ANS
-receives visceral afferents and is part of the larger visceral control system
-major regulator of MAP that tells ANS what to do


enteric nervous system

distinct division of ANS, contains more neurons than spinal cord
-includes myenteric and submucosal plexues of gut (diffuse interconnected series of neuronal cell bodies, axons, and dendrites)


myenteric (Auerbach's) plexus

controls motility


submucosal plexus

controls secretions


what in the gut is activated by distention and food?

mechanoreceptors and chemoreceptors in the epithelial lumen that innervate central control centers to activate PNS and inhibit SNS to promote digestion via enhanced motility and secretions


what happens when you cut the parasympathetic fibers innervating the gut?

decrease in GI muscle tone, increase in sphincter tone, showing that PNS exerts a tonic effect on GI motility


where are postganglionic neurons of PNS primarily located?

in myenteric and submucosal plexuses


where is PNS innervation of the GI system particularly extensive?

in the oral cavity and the anus
-smell/presence of food initiates nose/mouth to brain stem to salivate and secrete digestive juices
-distention in rectum initiates mechanoreceptors to sacral region of spinal cord to activate PNS defecation


PNS effect on myenteric plexus

activation is depolarizing, and generates APs leading to contractions of smooth muscle of gut


SNS effect on myenteric plexus

NE is released, which is hyperpolarizing and relaxing the smooth muscle, and increasing sphincter constriction
-too strong, can inhibit motility so much that movement of food is blocked (ileus)


actions of detrussor muscle, internal, and external sphincters in bladder filling

detrusor: relaxed via beta2 sympathetics
internal: contracted via alpha1 sympathetics
external: contracted via voluntary somatic


actions of detrussor muscle, internal, and external sphincters in bladder emptying

detrusor: contracted via muscarinic parasympathetics
internal: relaxed via muscarinic parasympathetics
external: relaxed via voluntary somatic


what are descending cortical pathways regulating through ANS?

fear, panic, stress and related responses
-may be via direct connections in spinal cord, or indirect through hypothalamus


examples in which visceral afferents overwhelm cortical function

nothing else seems to matter
-visceral pain
-bladder, bowel distention
-hypothermia, hyperthermia


vasovagal syncope

emotional fainting begins with disturbing thoughts in cortex
-activates vasodilator centers in hypothalamus and heart via vagus nerves, slowing heart
-signals through spinal cord to SNS vasodilator nerves in muscles (rapidly increasing flow to muscles)
-resultant fall in arterial pressure reduces blood flow to brain and causes person to lose consciousness

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