Autonomic Nervous System Flashcards
3 sympathetic nervous system activations
- chronotropic
- dromotropic
- inotropic
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
- chronotropic
- dromotropic
- inotropic
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
vasoconstriction
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
sweating
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
- hunger
- nausea
- dyspnea
- 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
