Autonomic Nervous System Basics Flashcards

Basics of ANS function, effects, and receptors

1
Q

What does the ANS regulate (3)

A
  1. the heart
  2. secretory glands
  3. smooth muscles
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2
Q

When does the SNS activate?

A

in acute, stressful situations
Exercise Excitement Emotions

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3
Q

SNS effect on the eyes

A

mydriasis - pupil dilation via contraction of the pupillary muscles

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4
Q

Mydriasis (meaning)

A

dilation of the pupil via contraction of the pupillary muscles = SNS effect

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5
Q

SNS effect on the brain

A

increased focus, attention (increased blood flow to brain)

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6
Q

SNS effect on the heart

A

increased HR and force of contraction

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7
Q

SNS effect on blood vessels

A

vasodilation OR vasoconstriction

some have adrenergic and some have cholinergic receptors (depends on which are stimulated)

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8
Q

SNS effects on the lungs

A

dilation of the bronchi
(allows increased airflow, maximizes oxygen)

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9
Q

SNS effects on the adrenal glands

A

stimulates the release of adrenaline and noradrenaline into the blood stream

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10
Q

SNS effects on the sex organs

A

increases reproductive success
a. ejaculation
b. contraction of the vagina
c. relaxation of the uterus

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11
Q

SNS effects on the urinary system

A

a. relaxation of the detrusor muscle
b. contraction of the internal urinary sphincter

**prevents urination/ urinary urgency

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12
Q

SNS effects on the digestive system

A

decreases gastrointestinal secretions and motility

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13
Q

SNS effect on liver/ adipose tissue

A

increase in glycogenolysis, lipolysis

**increase in release of stored energy substrates for conversion into energy

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14
Q

SNS effect on sweat glands

A

diaphoresis

**cool down muscles

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15
Q

SNS effect on coagulation

A

increased

**increased blood flow increases clotting agents available at any given location

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16
Q

SNS effect on kidneys

A

stimulates the release of renin

**renin release increases BP

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17
Q

Neurons of the SNS exit in the:

A

thoraco-lumbar region (T1-L2)

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18
Q

SNS neuron structure

A

short preganglionic
long postganglionic

= diffuse (generalized) effects

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19
Q

SNS post-ganglionic neuron features

A

can function as a:
a. neuron (releases NTs)
b. adrenal medulla (releases
hormones)

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20
Q

SNS produces _____ effects

A

diffuse (generalized) effects
d/t: long post-ganglionic
neuron releasing NTs and
adrenal medulla releasing
hormones

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21
Q

When does the PNS activate?

A

for maintenance functions of the body
Digestion Defecation Diuresis

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22
Q

PNS effect on the eyes

A

a. miosis - pupil contraction via relaxation of the pupillary iris muscle
b. accommodation - contraction of the ciliary muscle to allow for near vision

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23
Q

miosis (meaning)

A

relaxation of the pupillary iris muscle = PNS effect

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24
Q

accommodation (meaning)

A

contraction of the ciliary muscle allowing for near vision = PNS effect

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25
Q

PNS effect on the heart

A

reduced HR, slightly reduced force of contraction of the atria

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26
Q

PNS effect on the blood vessels

A

little to no effect –> largely SNS regulated

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27
Q

PNS effect on the lungs

A

a. bronchoconstriction (not as
much oxygen needed at rest)
b. increased secretions

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28
Q

PNS effect on adrenal glands

A

decrease secretions

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29
Q

PNS effect on sex organs

A

erection

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30
Q

PNS effect on urinary system

A

a. contraction of bladder
b. relaxation of the internal urinary sphincter

**allows for urination

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31
Q

PNS effect on the digestive system

A

stimulation of gastrointestinal motility, increased gastric secretions

**promotes emptying of bowels

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32
Q

Neurons of the PNS exit in the:

A

craniosacral region
a. cranial nerves III, VII, IX, X
b. Sacral nerves S2, S3, S4

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33
Q

Structure of the PNS neurons:

A

preganglionic neurons = long
preganglionic neurons = short

= localized effects

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34
Q

PNS produces _____ effects

A

localized
d/t: short post-ganglionic neurons

35
Q

all pre-ganglionic neurons (PNS and SNS) release:

A

Acetylcholine

36
Q

post-ganglionic sympathetic neurons interacting with various organs release:

A

Norepinephrine/ Noradrenaline

37
Q

post-ganglionic sympathetic neurons interacting with sweat glands relase:

A

Acetylcholine

38
Q

the adrenal medulla secrets:

A

20% norepinephrine
80% epinephrine

39
Q

post-ganglionic parasympathetic neurons interacting with various organs release:

A

acetylcholine

40
Q

Synthesis of Adrenergic NTs –> Adrenaline

A
  1. Tyrosine
  2. DOPA
  3. Dopamine
  4. Noradrenaline
  5. Adrenaline
41
Q

Synthesis of Adrenergic NTs –> Noradrenaline

A
  1. Tyrosine
  2. DOPA
  3. Dopamine
  4. Noradrenaline
42
Q

Where does the conversion of Noradrenaline into Adrenaline occur?

A

In the adrenal glands

43
Q

What are Noradrenaline and Adrenaline released as? (hormone vs NT)

A

Noradrenaline = hormone
Adrenaline = NT

44
Q

Noradrenaline Pathway

A
  1. Tyrosine
  2. DOPA
  3. Dopamine
  4. Norepinephrine stored in
    vesicles
  5. Norepinephrine released into
    synaptic gap
45
Q

Action of NE when released

A

a. bind to A2 receptor on preganglionic neurons

b. bind to A1 or B1-3 on postganglionic neurons

46
Q

Recycling of NE (process)

A

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)

47
Q

Inactivation of NE (process)

A

undergoes reuptake at the level of the preganglionic –> broken down (inactivated) by MAO if not in vesicles

48
Q

Adrenergic Metabolites

A

VMA and MOPEG

** both urinary

49
Q

Urinary VMA

A

metabolite produced from noradrenaline released in the periphery (in the body(

** high levels usually occur as a result of tumors

50
Q

Urinary MOPEG

A

metabolite produced from noradrenaline released by neurons in the brain

51
Q

Drugs Affecting Adrenergic Neurotransmission: Synthesis Inhibitors

A

Alpha Methyl Tyrosine

–> competes with tyrosine as a precursor to NA/NE

RESULT: dec NA/NE production = dec sympathetic effects

52
Q

Drugs Affecting Adrenergic Neurotransmission: Inhibition of NE Storage

A

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

53
Q

Drugs Affecting Adrenergic Neurotransmission: Displacement

A

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

54
Q

Drugs Affecting Adrenergic Neurotransmission: Inhibition of release

A

Guanethidine

prevents NA/NE from being released

RESULT: dec sympathetic effects

55
Q

Drugs Affecting Adrenergic Neurotransmission: Beta-1 adrenergic antagonists

A

Metroprolol

RESULT: blocks sympathetic effect (dec effects)

56
Q

Drugs Affecting Adrenergic Neurotransmission: Beta-1 Adrenergic Agonists

A

Dobutamine

RESULT: increases sympathetic effect

57
Q

Drugs Affecting Adrenergic Neurotransmission: Reuptake Inhibitors

A

Cocaine, Tricyclic Antidepressants

forces NA/NE to remain in synaptic gap for longer by inhibiting mechanisms that cause reuptake

RESULT: increased sympathetic effect

58
Q

Drugs Affecting Adrenergic Neurotransmission: MAO Inhibitors

A

Pargyline

Inhibits MAO, allowing reabsorbed NA/NE to be placed in vesicles to be reused rather than be inactivated

RESULT: increased sympathetic effects

59
Q

Acetylcholine Synthesis

A

Acetyl CoA + Choline = Acetylcholine

60
Q

What molecule combines Acetyl CoA and Choline?

A

Choline Acetyltransferase (ChAT)

61
Q

What molecule breaks down Acetylcholine?

A

Acetylcholinesterase (AChE)
- choline is reabsorbed into the
preganglionic neuron to be
reused
- acetate leaves the synaptic
gap to be destroyed

62
Q

Drugs Affecting Cholinergic Neurotransmission: Reuptake Inhibitors

A

Hemicholinium

Prevents choline from being reabsorbed after being broken down by AChE –> decreased choline available to create new ACh

Result: dec action

63
Q

Drugs Affecting Cholinergic Neurotransmission: Storage Inhibitors

A

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

64
Q

Drugs Affecting Cholinergic Neurotransmission: Displacement

A

Latrotoxin (Black Widow Venom)

  1. Initially causes stored ACh to be released so that latrotoxin can take its place in the vesicles –> initial efflux of ACh (inc effects)
  2. Prevents new ACh synthesis –> dec effects

RESULTS: initial increased effect, then decreased effect long term

65
Q

Drugs Affecting Cholinergic Neurotransmission: Inhibitor of Release

A

Botulinum Toxin

inhibit’s ACh’s ability to leave vesicles

RESULT: decreased action

66
Q

Drugs Affecting Cholinergic Neurotransmission: Muscarinic Receptor Agonists

A

Muscarine

stimulates muscarinic cholinergic receptors

RESULT: inc action

67
Q

Drugs Affecting Cholinergic Neurotransmission: Muscarinic Receptor Antagonist

A

Atropine

blocks muscarinic cholinergic receptors

RESULT: decreased effect

68
Q

Drugs Affecting Cholinergic Neurotransmission: Acetylcholinesterase (AChE) inhibitors

A

Nerve Gasses

inhibits enzymatic breakdown of ACh by AChE resulting in increased quantities of acetylcholine remaining in synapse

RESULT: increased action

69
Q

Cholinergic Receptor Types

A

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

70
Q

Where are Nn receptors located?

A

all postganglionic neurons (SNS and PNS) including adrenal medulla

71
Q

Where are Nm receptors located?

A

skeletal muscle

72
Q

Where are M receptors located?

A

smooth muscle (PNS) and glands (SNS)

73
Q

Adrenergic Receptor Types

A

Alpha and Beta Receptors
- receptors on various organs of
sympathetic system

74
Q

Alpha 1 Receptors

A

(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)

75
Q

Alpha 2 Receptors

A

(negative feedback)

Tissue/Target + Function
a. presynaptic - inhibits NA release to dec A1 stimulation
b. pancreas - dec insulin secretions
c. gastrointestinal tract - dec secretion

76
Q

Beta 1 Receptors

A

(1 heart + kidneys)

Tissue/Target + Function
a. heart - inc HR and force of contraction
b. kidneys - release of renin (inc BP)

77
Q

Beta 2 Receptors

A

(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

78
Q

Beta 3 Receptors

A

(relaxation + metabolic effects)

Tissue/Target + Function
a. adipose tissue - lipolysis
b. bladder (detrusor) - relaxation

79
Q

Nicotinic Neuronal (Nn) Receptors

A

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)

80
Q

Nicotinic Muscular (Nm) Receptors

A

skeletal muscles - contraction

81
Q

Muscarinic M1, M4, M5 Receptors

A

brain - effects according to neuronal pathway

82
Q

Muscarinic M2 Receptors

A

heart muscle - decreased HR + force of contraction (atria)

83
Q

Muscarinic M3 Receptors

A

a. smooth muscle, glands - stimulation of parasympathetic effects (inc secretions, contractions)

b. eyes - miosis + accommodation

c. sweat glands - stimulation of diaphoresis

84
Q

What system stimulates sweat glands?

A

Muscarinic receptors (ACh) stimulated by SNS