Autonomic Nervous System Basics Flashcards
Basics of ANS function, effects, and receptors
What does the ANS regulate (3)
- the heart
- secretory glands
- smooth muscles
When does the SNS activate?
in acute, stressful situations
Exercise Excitement Emotions
SNS effect on the eyes
mydriasis - pupil dilation via contraction of the pupillary muscles
Mydriasis (meaning)
dilation of the pupil via contraction of the pupillary muscles = SNS effect
SNS effect on the brain
increased focus, attention (increased blood flow to brain)
SNS effect on the heart
increased HR and force of contraction
SNS effect on blood vessels
vasodilation OR vasoconstriction
some have adrenergic and some have cholinergic receptors (depends on which are stimulated)
SNS effects on the lungs
dilation of the bronchi
(allows increased airflow, maximizes oxygen)
SNS effects on the adrenal glands
stimulates the release of adrenaline and noradrenaline into the blood stream
SNS effects on the sex organs
increases reproductive success
a. ejaculation
b. contraction of the vagina
c. relaxation of the uterus
SNS effects on the urinary system
a. relaxation of the detrusor muscle
b. contraction of the internal urinary sphincter
**prevents urination/ urinary urgency
SNS effects on the digestive system
decreases gastrointestinal secretions and motility
SNS effect on liver/ adipose tissue
increase in glycogenolysis, lipolysis
**increase in release of stored energy substrates for conversion into energy
SNS effect on sweat glands
diaphoresis
**cool down muscles
SNS effect on coagulation
increased
**increased blood flow increases clotting agents available at any given location
SNS effect on kidneys
stimulates the release of renin
**renin release increases BP
Neurons of the SNS exit in the:
thoraco-lumbar region (T1-L2)
SNS neuron structure
short preganglionic
long postganglionic
= diffuse (generalized) effects
SNS post-ganglionic neuron features
can function as a:
a. neuron (releases NTs)
b. adrenal medulla (releases
hormones)
SNS produces _____ effects
diffuse (generalized) effects
d/t: long post-ganglionic
neuron releasing NTs and
adrenal medulla releasing
hormones
When does the PNS activate?
for maintenance functions of the body
Digestion Defecation Diuresis
PNS effect on the eyes
a. miosis - pupil contraction via relaxation of the pupillary iris muscle
b. accommodation - contraction of the ciliary muscle to allow for near vision
miosis (meaning)
relaxation of the pupillary iris muscle = PNS effect
accommodation (meaning)
contraction of the ciliary muscle allowing for near vision = PNS effect
PNS effect on the heart
reduced HR, slightly reduced force of contraction of the atria
PNS effect on the blood vessels
little to no effect –> largely SNS regulated
PNS effect on the lungs
a. bronchoconstriction (not as
much oxygen needed at rest)
b. increased secretions
PNS effect on adrenal glands
decrease secretions
PNS effect on sex organs
erection
PNS effect on urinary system
a. contraction of bladder
b. relaxation of the internal urinary sphincter
**allows for urination
PNS effect on the digestive system
stimulation of gastrointestinal motility, increased gastric secretions
**promotes emptying of bowels
Neurons of the PNS exit in the:
craniosacral region
a. cranial nerves III, VII, IX, X
b. Sacral nerves S2, S3, S4
Structure of the PNS neurons:
preganglionic neurons = long
preganglionic neurons = short
= localized effects
PNS produces _____ effects
localized
d/t: short post-ganglionic neurons
all pre-ganglionic neurons (PNS and SNS) release:
Acetylcholine
post-ganglionic sympathetic neurons interacting with various organs release:
Norepinephrine/ Noradrenaline
post-ganglionic sympathetic neurons interacting with sweat glands relase:
Acetylcholine
the adrenal medulla secrets:
20% norepinephrine
80% epinephrine
post-ganglionic parasympathetic neurons interacting with various organs release:
acetylcholine
Synthesis of Adrenergic NTs –> Adrenaline
- Tyrosine
- DOPA
- Dopamine
- Noradrenaline
- Adrenaline
Synthesis of Adrenergic NTs –> Noradrenaline
- Tyrosine
- DOPA
- Dopamine
- Noradrenaline
Where does the conversion of Noradrenaline into Adrenaline occur?
In the adrenal glands
What are Noradrenaline and Adrenaline released as? (hormone vs NT)
Noradrenaline = hormone
Adrenaline = NT
Noradrenaline Pathway
- Tyrosine
- DOPA
- Dopamine
- Norepinephrine stored in
vesicles - Norepinephrine released into
synaptic gap
Action of NE when released
a. bind to A2 receptor on preganglionic neurons
b. bind to A1 or B1-3 on postganglionic neurons
Recycling of NE (process)
undergoes reuptake at the level of the preganglionic neuron –> will be stored in vesicles for future use
** will be inactivated by MAO in neuronal space (if not in vesicles)
Inactivation of NE (process)
undergoes reuptake at the level of the preganglionic –> broken down (inactivated) by MAO if not in vesicles
Adrenergic Metabolites
VMA and MOPEG
** both urinary
Urinary VMA
metabolite produced from noradrenaline released in the periphery (in the body(
** high levels usually occur as a result of tumors
Urinary MOPEG
metabolite produced from noradrenaline released by neurons in the brain
Drugs Affecting Adrenergic Neurotransmission: Synthesis Inhibitors
Alpha Methyl Tyrosine
–> competes with tyrosine as a precursor to NA/NE
RESULT: dec NA/NE production = dec sympathetic effects
Drugs Affecting Adrenergic Neurotransmission: Inhibition of NE Storage
Risperidone
decreases amount of NA/NE stored in vesicles after production/ reabsorption (exposed to MOA for inactivation –> less to be released
RESULT: dec NA/NE stored = dec sympathetic effects
Drugs Affecting Adrenergic Neurotransmission: Displacement
Amphetamines
displaces stored NA/NE from vesicles (amphetamines takes place in vesicles instead) –> massive efflux of NA/NE at once (too much for MOA to deactivate or to reuptake)
RESULT: increased sympathetic effects
Drugs Affecting Adrenergic Neurotransmission: Inhibition of release
Guanethidine
prevents NA/NE from being released
RESULT: dec sympathetic effects
Drugs Affecting Adrenergic Neurotransmission: Beta-1 adrenergic antagonists
Metroprolol
RESULT: blocks sympathetic effect (dec effects)
Drugs Affecting Adrenergic Neurotransmission: Beta-1 Adrenergic Agonists
Dobutamine
RESULT: increases sympathetic effect
Drugs Affecting Adrenergic Neurotransmission: Reuptake Inhibitors
Cocaine, Tricyclic Antidepressants
forces NA/NE to remain in synaptic gap for longer by inhibiting mechanisms that cause reuptake
RESULT: increased sympathetic effect
Drugs Affecting Adrenergic Neurotransmission: MAO Inhibitors
Pargyline
Inhibits MAO, allowing reabsorbed NA/NE to be placed in vesicles to be reused rather than be inactivated
RESULT: increased sympathetic effects
Acetylcholine Synthesis
Acetyl CoA + Choline = Acetylcholine
What molecule combines Acetyl CoA and Choline?
Choline Acetyltransferase (ChAT)
What molecule breaks down Acetylcholine?
Acetylcholinesterase (AChE)
- choline is reabsorbed into the
preganglionic neuron to be
reused
- acetate leaves the synaptic
gap to be destroyed
Drugs Affecting Cholinergic Neurotransmission: Reuptake Inhibitors
Hemicholinium
Prevents choline from being reabsorbed after being broken down by AChE –> decreased choline available to create new ACh
Result: dec action
Drugs Affecting Cholinergic Neurotransmission: Storage Inhibitors
Vesamicol
Formed ACh is prevented from being stored in vesicles, susceptible to being broken down by Acetylcholinesterase –> less ACh stored in vesicles to be released
Result: dec action
Drugs Affecting Cholinergic Neurotransmission: Displacement
Latrotoxin (Black Widow Venom)
- Initially causes stored ACh to be released so that latrotoxin can take its place in the vesicles –> initial efflux of ACh (inc effects)
- Prevents new ACh synthesis –> dec effects
RESULTS: initial increased effect, then decreased effect long term
Drugs Affecting Cholinergic Neurotransmission: Inhibitor of Release
Botulinum Toxin
inhibit’s ACh’s ability to leave vesicles
RESULT: decreased action
Drugs Affecting Cholinergic Neurotransmission: Muscarinic Receptor Agonists
Muscarine
stimulates muscarinic cholinergic receptors
RESULT: inc action
Drugs Affecting Cholinergic Neurotransmission: Muscarinic Receptor Antagonist
Atropine
blocks muscarinic cholinergic receptors
RESULT: decreased effect
Drugs Affecting Cholinergic Neurotransmission: Acetylcholinesterase (AChE) inhibitors
Nerve Gasses
inhibits enzymatic breakdown of ACh by AChE resulting in increased quantities of acetylcholine remaining in synapse
RESULT: increased action
Cholinergic Receptor Types
Nicotinic (Nn and Nm)
- located on postganglionic
neurons of sympathetic and
parasympathetic systems (all)
- acts as receptors on skeletal
muscle and adrenal medulla
Muscarinic (M)
- acts as receptors on smooth
muscle and glands of
parasympathetic system
Where are Nn receptors located?
all postganglionic neurons (SNS and PNS) including adrenal medulla
Where are Nm receptors located?
skeletal muscle
Where are M receptors located?
smooth muscle (PNS) and glands (SNS)
Adrenergic Receptor Types
Alpha and Beta Receptors
- receptors on various organs of
sympathetic system
Alpha 1 Receptors
(point and shoot)
Tissue/Target + Function
a. Blood Vessels (skin/ splenic)- vasoconstriction
b. Internal Urinary Sphincter - contraction (close)
c. Penis - ejaculation
d. Piloerector muscles (hair) - contraction
e. Salivary glands - thick mucoid secretions (dec salivation)
f. Eye - mydriasis (dilation)
Alpha 2 Receptors
(negative feedback)
Tissue/Target + Function
a. presynaptic - inhibits NA release to dec A1 stimulation
b. pancreas - dec insulin secretions
c. gastrointestinal tract - dec secretion
Beta 1 Receptors
(1 heart + kidneys)
Tissue/Target + Function
a. heart - inc HR and force of contraction
b. kidneys - release of renin (inc BP)
Beta 2 Receptors
(2 lungs - relaxation/ dilation, metabolic effects)
Tissue/Target + Function
a. lungs - relaxation of the bronchi = bronchodilation
b. uterus, bladder - relaxation
c. blood vessels (skeletal/ coronaries) - dilation
d. liver + skeletal muscle - glycogenolysis/ gluconeogenesis
e. pancreas - increased insulin secretion
f. GI tract - decreased motility, dec secretions
Beta 3 Receptors
(relaxation + metabolic effects)
Tissue/Target + Function
a. adipose tissue - lipolysis
b. bladder (detrusor) - relaxation
Nicotinic Neuronal (Nn) Receptors
a. SNS/ PNS postganglionic neurons - stimulation leads to increased signaling in both systems
b. adrenaline glands - epi and norepi released as hormones in bloodstream (4:1 ratio)
Nicotinic Muscular (Nm) Receptors
skeletal muscles - contraction
Muscarinic M1, M4, M5 Receptors
brain - effects according to neuronal pathway
Muscarinic M2 Receptors
heart muscle - decreased HR + force of contraction (atria)
Muscarinic M3 Receptors
a. smooth muscle, glands - stimulation of parasympathetic effects (inc secretions, contractions)
b. eyes - miosis + accommodation
c. sweat glands - stimulation of diaphoresis
What system stimulates sweat glands?
Muscarinic receptors (ACh) stimulated by SNS