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Pharmacology > PNS General + Cholinergic > Flashcards

PNS General + Cholinergic Flashcards

1
Q

Characteristics of the Autonomic Nervous

System

A

􀁺 Largely involuntary

􀁺 Innervates everything except skeletal muscle

􀁺 Controls visceral functions necessary for life: 
􀁺 Cardiac output
􀁺 Blood flow to organs
􀁺 Metabolism
􀁺 Gastrointestinal motility
􀁺 Urogenital functions
􀁺 Body temperature
􀁺 Sweating
􀁺 Endocrine gland secretions
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2
Q

Parasympathetic

A

􀁺 Preganglionic neurons arise in CNS, send axons out through the spinal cord from the cranial and sacral spinal nerves

􀁺 Axons synapse in peripheral ganglia; most ganglia are close to or within the walls of the innervated organs but some ganglia are located outside the organs innervated

􀁺 Postganglionic neurons arise within ganglia, send axons out to synapse at
end organs

􀁺 Discrete output

LONG Pre-ganglionic
SHORT post-ganglionic

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3
Q

Sympathetic

A

􀁺 Preganglionic neurons arise in CNS, send axons out through the spinal cord from the thoracic and lumbar spinal nerves

􀁺 Axons synapse in 3 prevertebral ganglia (celiac, superior mesenteric, and
inferior mesenteric) or in 22 pairs of paravertebral ganglia located along the
spinal cord

􀁺 Postganglionic neurons arise within ganglia, send axons out to synapse at
end organs

􀁺 Distributed output

SHORT Pre-ganglionic
LONG post-ganglionic

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4
Q

Organs w/dual innervation

A 
􀁺 Eye
􀁺 Heart
􀁺 Bronchial tree
􀁺 Gastrointestinal tract
􀁺 Salivary glands
􀁺 Urinary bladder
􀁺 Sex organs
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5
Q

Organs with ONLY sympathetic innervation

A

􀁺 Blood vessels
􀁺 Spleen
􀁺 Piloerector muscles
􀁺 Sweat glands

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6
Q

Flight or fight response

A

Sympathetic Response:

  • dilate pupil (mydriasis)
  • decrease saliva
  • increase HR
  • dilates bronchi
  • inhibits peristalsis and secretion
  • increase glycogenolysis in liver (we need glucose)
  • secrete epi and NE
  • inhibit bladder contraction
  • vasodilation to skeletal muscles
  • vasoconstriction elsewhere
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7
Q

Rest and Digest Response

A

Parasympathetic Response:

  • Pupil constriction (miosis)
  • Slow HR
  • Increase saliva
  • Increase peristalsis and secretion
  • Release of bile
  • Contracts bladder
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8
Q

Cholinergic NT System

A

􀁺 Cholinergic: neurons that release ACh:

  1. All motor neurons to skeletal muscle (somatic nerves)
  2. All preganglionic ANS neurons; first synapse in ANS is always
    cholinergic
  3. All postganglionic parasympathetic neurons
  4. Some postganglionic sympathetic neurons
    􀁺 Most sweat glands
    􀁺 Some blood vessels in skeletal muscle
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9
Q

Adrenergic NT System

A

􀁺 Adrenergic: neurons that release catecholamines: NE, Epi, DA

  1. Most postganglionic sympathetic neurons release NE
  2. Adrenal medulla (a modified sympathetic ganglion) releases E and
    NE
  3. Some postganglionic neurons release DA
    -especially in venous system
    -renal SMC (dilation to increase RBF)
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10
Q

2 Ways to get a cholinergic post-ganglionic sympathetic neuron (remember most post sympa are noradrenergic)

A
  1. Target-dependent noradrenergic/cholinergic switch
  2. Target-independent cholinergic differentiation
    - started that way

*Slide 21

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11
Q

Describe the 1st synapse in all of the autonomic NS

A

All preganglionic ANS neurons; first synapse in ANS is always
cholinergic!!!

The postganglionic receptor is always a Nicotinic ACh receptor

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12
Q

Biosynthesis of ACh

Slide 23

A

*In the pre-ganglionic neuron

Choline + acetyl co-A =ACh

enzyme: ChAT: choline-acetyl transferase

*ACh transported into vesicle via VAT (driven by H+ grandient)
(slide 24)

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13
Q

Metabolism of ACh

Slide 23

A

ACh –> acetate + choline

  • Occurs in the synapse
  • Enzyme: AChE: Acetylcholine esterase
  • choline taken back up via Na+ dependent transporter (Slide 24)
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14
Q

Catecholamine biosynthesis

Slide 25

A

Tyrosine + TH (Tyrosine Hydroxlase) –> DOPA

DOPA + AAAD (Aromatic amino decarboxylase) –> dopamine

Dopamine + DBH (Dopamine B Hydroxylase) –> NE

NE + PNMT (phenylethanolamine N-methyl transferase) –> Epi

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15
Q

Enzymes used in catecholamine metabolism

A

Phase I: MAO, ALDH

Phase II: COMT

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16
Q

Vanillylmandelic Acid (VMA)

A

Product of NE/Epi metabolism

Urine Marker for NE/EPi

Used to dx pheochromocytoma (a lot of VMA)

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17
Q

Adrenergic Synapse

Slide 28

A
  1. VMAT: vesicle monamine transporter
    ◦ transports DA into vesicle
    ◦ There are 2 VMATs
    ‣ VMAT2 most common
  2. In contrast to ACh, NE is re-taken back
    into the cell via NET
    ◦ There’s also a SERT and DET (for serotonin and DA)
    ◦ Important targets for certain drugs
    like anti-depressants, psychoactives
    ◦ Cocaine blocks NET, SERT, DET
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18
Q

Receptors of the PNS (peripheral)

A

2 cholinergic receptors

3 adrenergic receptors

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19
Q

Receptors of the PNS:

􀁺 Two types of cholinergic receptors

A
  1. Muscarinic receptors
    􀁺 G protein-coupled

􀁺 Respond to the plant alkaloid muscarine

􀁺 Five subtypes (M1-M5)
**In PNS M1-M3 are the most important, with M2 and M3 doing 90%

  1. Nicotinic receptors
    􀁺 Ligand-gated ion channels
    • Basically Na+/K+ pentameric channels

􀁺 Respond to the plant alkaloid nicotine

􀁺 Two subtypes
• Nm-skeletal muscle
• Nn-neuronal (on post-ganglionic)

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20
Q

Receptors of the PNS:

􀁺 Three types of adrenergic receptors respond to catecholamines

A

* all G protein-coupled*

  1. Two types of receptors respond to NE and E
    􀁺 alpha receptors, two subtypes (a1, a2); each subtype has three subtypes (a1A, a1B,
    a1D and a2A, a2B, a2C)

􀁺 B receptor, three subtypes (B1-B3)

  1. One type of receptor responds to DA
    􀁺 Five subtypes (D1-D5)
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21
Q

PNS cholinergic receptor: M2

A 
Tissue: Heart and 
Axon terminals (autoreceptors)

Response: ↓ Heart rate, conduction velocity,
contractility

Mechanism: ↓ AC → ↓ cAMP; ↑ K+ channel
efflux, ↓ Ca++ channel influx

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22
Q

PNS cholinergic receptor: M1

A

Tissue: Autonomic ganglia

Response: Depolarizes postsynaptic
neurons (slow EPSP)

Mechanism: ↑ PLC → ↑ IP3, DAG, Ca++
(Gq)

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23
Q

PNS cholinergic receptor: M3

A 
1. Tissue: Smooth muscle (eye,bronchioles, GI tract, urogenital
system)
Response: Contraction
Mechanism: ↑ PLC → ↑ IP3, DAG, Ca++
(Gq)
  1. Tissue: Secretory glands
    Response: ↑ Secretion
    Mechanism: ↑ PLC → ↑ IP3, DAG, Ca++
    (Gq)
3. Tissue: Vascular endothelium
Response: Dilates blood vessels
-this is from local ACh b/c remember that PNS doesn't innervate vasculature 
Mechanism: Ca++/CaM activates eNOS →
↑ NO → ↑ cGMP → relaxation
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24
Q

PNS cholinergic receptor: Nm

A

Tissue: Neuromuscular junction

Response: Skeletal muscle contraction

Mechanism: Opens Na+/K+ channels →
depolarization

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25
Q

PNS cholinergic receptor: Nn

A
  1. Tissue: Autonomic ganglia
    Response: Depolarizes postsynaptic neurons
  2. Tissue: Adrenal medulla
    Response: Depolarizes medullary cells →
    secretion of catecholamines

For both: Mechanism: Opens Na+/K+ channels →depolarization

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26
Q

PNS adrenergic receptor: a1

A

Mechanism: ↑ PLC → ↑ IP3, DAG, Ca++

  1. Tissue: Smooth muscle (eye, vascular,
    urogenital, hair follicles)
    Response: Contracts smooth muscle (Increase BP, or keep it up enough to perfuse)
  2. Tissue: Liver
    Response: ↑ Glycogenolysis, gluconeogenesis
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27
Q

PNS adrenergic receptor: a2

A

Mechanism:
↓ AC → ↓ cAMP; ↑ K+ channel efflux (via Gβγ); ↓ L- and N type
Ca++ channel influx; ↑
PLC → ↑ IP3, DAG, Ca++

  1. Tissue: Axon terminals (autoreceptors)
    Response: ↓ NE release
  2. Tissue: Pancreatic b cells
    Response: ↓ Insulin release
  3. Tissue: Vascular smooth muscle
    Response: Contracts smooth muscle (Increase BP, or keep it up enough to perfuse)
  4. Tissue: Platelets
    Response: Aggregation
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28
Q

PNS adrenergic receptor: B1

A

Mechanism:
↑ AC → ↑ cAMP → ↑ PKA →↑ L-type Ca++ channel influx

  1. Tissue: Heart
    Response: ↑ Heart rate, conduction velocity, contractility
  2. Tissue: Kidney (juxtaglomerular cells)
    Response: ↑ Renin release
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29
Q

PNS adrenergic receptor: B2

A

Mechanism:
↑ AC → ↑ cAMP;

in smooth muscle, inhibits MLCK → ↓ myosin-PO4 → relaxation

  1. Tissue: Smooth muscle (eye, bronchioles,
    GI, urogenital, vascular)
    Response: Relaxes smooth muscle
  2. Tissue: Heart
    Response: ↑ Heart rate, contractility
  3. Tissue: Liver and skeletal muscle
    Response: ↑Glycogenolysis, gluconeogenesis (liver)
  4. Tissue: Pancreatic b cells
    Response: ↑ Insulin release
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30
Q

PNS adrenergic receptor: B3

A

Tissue: Lipocytes

Response: activates lipolysis

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31
Q

PNS adrenergic receptor: D1

A

Tissue: Vascular smooth muscle, especially
renal vasculature

Response: Dilates blood vessels, increasing RBF thus increasing GFR

Mechanism:
↑ AC → ↑ cAMP

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32
Q

PNS adrenergic receptor: D2

A

Tissue: Axon terminals (autoreceptors) and
Cholinergic neurons in the gut

Response:
↓ DA release
↓ GI motility

Mechanism:
↑ AC → ↑ cAMP;
↑ K+ efflux; ↓Ca++ influx

33
Q

Eye Pupil Diameter

Slide 33

A 
1. Iris circular muscle
􀁺 M3 activation → muscle contraction →
miosis
􀁺 β2 activation → muscle relaxation →
mydriasis (slight effect)
-eases the way for a1
  1. Iris radial muscle
    􀁺 α1 activation → muscle contraction →mydriasis
34
Q

Eye Lens Shape (Slide 34)

A
  1. Ciliary smooth muscle:

􀁺 M3 activation → muscle
contraction → relaxes
ligament → accommodation for
near vision (rest and read)

􀁺 β2 activation → muscle
relaxation → stretches
ligament (slight effect)
-flat lens for distance sight

35
Q

Eye secretion

A
  1. Lacrimal glands

􀁺 M3 (ACh) activation → lacrimation

36
Q

Lung (Slide 35)

  1. Bronchial Smooth Muscle
  2. Bronchial Glands
A 
1.  Bronchial smooth muscle
􀁺 M3 activation → muscle
contraction →
bronchoconstriction
􀁺 β2 activation → muscle
relaxation →
bronchodilation
2. Bronchial glands
􀁺 M3 activation → mucous secretion
􀁺 β2 activation → watery
secretion via CFTR
activation
37
Q

CV: Heart

A 
􀁺 Vagal Tone:
M2 activation → bradycardia (SA node), ↓ AV node conductivity,
↓ atrial contractility
*only in atria 
*overall relaxing effect

􀁺 β1 and β2 activation → tachycardia (SA node), ↑ AV node automaticity and conductivity, ↑ His-Purkinje automaticity and
conductivity, ↑ ventricular automaticity and contractility

38
Q

CV: Vascular System

A

􀁺 M3 activation (endothelial cells) → relaxation → ↓ blood pressure

􀁺 α1 and α2 activation (smooth muscle cells) → constriction → ↑
blood pressure

􀁺 β2 activation (liver and skeletal muscle) → relaxation → ↓ TPR →
↑ blood flow to these tissues

􀁺 D1 activation → dilation of renal arteries and arterioles → ↑ renal
blood flow

39
Q

Muscarinic NT on the heart (See slide 38 now)

A

Overall ACh relaxes the heart

  • Decreased cAMP results in less current through If (I funny)
  • decreases rate of depolarization
  • leads to slowed HR

• ACh binds to M2R and then Beta gamma subunits act upon Ik to activate it and more K+ leaves the cell and causes hyperpolarization–>relaxing effect

Decreased PKA–>decreased
Phosphorylation of L-Ca2+ channels–> decreased contractility–>conduction–>Heart rate

40
Q

Beta activation of the heart (See Slide 39 now)

A

Excitatory:

Gprotein

Increases cAMP activates PK

PK phosphorylates L-type Ca2+ channel

Increases HR, conduction velocity, force of contraction

41
Q

Explain the innervation of the vascular system

A
  1. Innervated by the SYMPATHETIC NS
  2. Not innervated by parasymp.
  3. Although no neurons, ACh still has influence
  4. Because there is ChAT activity on vasculature allowing for local production of ACh
  5. May perhaps be stretch activated
42
Q

Describe the control of the vascular smooth muscle cells at rest and during flight.
(slide 43)

A
  1. Rest: only NE
    - alpha-1 Receptors for NE control
    - vasoconstriction of vascular SMCs
    - this is balanced with vasodilation from ACh MR action on endothelial cells
  2. Flight: Epi
    -B2 receptors in liver and skeletal muscle cause relaxation
    -↓ TPR →
    ↑ blood flow to these tissues
43
Q

Intestine

A
  1. M3 activation → contraction of circular and longitudinal muscles in intestinal walls →
    ↑ motility
  2. α1 and β2 activation → muscle relaxation→ ↓ motility
    􀁺 In GI smooth muscle, hyperpolarization and relaxation is caused by
    activation of calcium-dependent K+ efflux channels
44
Q

Gastrointestinal Sphincters

A

􀁺 M3 activation → relaxation

􀁺 α1 activation → contraction

45
Q

GI secretions

A
  1. M3 activation → ↑ acid secretion from parietal cells, ↑ secretions from gastric and intestinal glands, gall bladder contraction

􀁺 β2 activation → ↓ gastric acid secretion, relaxes gall bladder, ↑amylase secretion (want more free glucose)

46
Q

Where are these receptors located in the GI tract?

  1. M3
  2. a1, B2

(Slide 45)

A
  1. • M3 (ACh) receptors of the PNS are in the glands
    of the mucosa and submucosa, and in the circular
    and longitudinal muscle
    ◦ promotes peristalsis
  2. SNS receptors (adrenergic)
    are in the circular and
    longitudinal muscle
47
Q

Kidney and bladder

Slide 47

A

􀁺 D1 activation → vasodilation → ↑ blood flow, GFR

􀁺 β1 activation → stimulates renin release from kidney

􀁺 M3 activation → contraction of bladder detrusor, relaxation of trigone and sphincter → promotes urination

􀁺 β2 activation → relaxes detrusor → urinary retention

􀁺 α1 activation → constricts trigone and sphincter → urinary retention

48
Q

Penis

A

**Rare example of SNS and PSNS working together to stimulate!

􀁺 M3 activation → relaxation of vessels → erection

􀁺 α1 activation → contraction of seminal vesicles, prostatic capsule, vas deferens → ejaculation

49
Q

Uterus

A
  1. Nonpregnant: β2 activation → relaxes uterus
  2. Pregnant
    ***Rare example of SNS and PSNS working together to stimulate!
    􀁺 M3 activation → contracts uterus
    􀁺 α1 activation → contracts uterus

􀁺 β2 activation → relaxes uterus

50
Q

Secretion

A
  1. M3 activation → stimulates watery secretions from salivary, nasopharyngeal, pulmonary, gastrointestinal, and eccrine sweat glands
  2. α1 activation → stimulates secretion from apocrine sweat glands found in axillary and pubic regions; produces viscous salivary
    secretions
51
Q

Metabolism

A

􀁺 α2 activation → ↓ insulin release from pancreatic b cells

􀁺 β2 activation → promotes glycogenolysis and gluconeogenesis in
liver, glycogenolysis and K+ uptake in skeletal muscle, ↑ insulin release from pancreatic β cells
-Want glucose available and insulin so skeletal muscles can take glu in

􀁺 β3 activation → stimulates lipolysis in adipocytes

52
Q

Predominant tone of the body?

A

Mainly run on ACh except vasculature. Overall body is under the control of the PSNS

53
Q

Predominant tone of:

Arterioles and Veins

A

Sympathetic (adrenergic)

54
Q

Predominant tone of:

Sweat glands

A

Sympathetic (cholinergic)

55
Q

Predominant tone of:

Heart

A

Parasympathetic (cholinergic

56
Q

Predominant tone of:

Iris

A

Parasympathetic (cholinergic

57
Q

Predominant tone of:

Ciliary Muscle

A

Parasympathetic (cholinergic

58
Q

Predominant tone of:

GI Tract

A

Parasympathetic (cholinergic

59
Q

Predominant tone of:

Urinary Bladder

A

Parasympathetic (cholinergic

60
Q

Predominant tone of:

Salivary glands

A

Parasympathetic (cholinergic

61
Q

Summary of SNS

A

􀁺 Prepares for strenuous activity, mobilizes energy stores (fight or flight)

􀁺 Widespread output

􀁺 ↑ Pupil diameter, ↑ respiration, ↑ heart rate, ↑ blood pressure, ↓
GI motility and secretions, ↓ urination, ↑ sweating

62
Q

Summary of PSNS

A

􀁺 Accumulation and conservation of energy (rest and digest)

􀁺 Discrete output

􀁺 Maintenance functions during periods of minimal activity

􀁺 ↓ Pupil diameter, accommodation for near vision, ↑ lacrimation, ↓
respiration, ↓ heart rate, ↓ blood pressure, ↑ GI motility and secretions, ↑ urination

63
Q

Cholinergic Drug classes

A

􀁺 Cholinomimetic drugs: drugs that mimic ACh activity

􀁺 Cholinolytic drugs: drugs that inhibit ACh activity

64
Q

􀁺 Cholinomimetic drugs: drugs that mimic ACh activity

A

􀁺 Muscarinic agonists: M receptor agonists
􀁺 Nicotinic agonists: N receptor agonists
􀁺 Drugs that slow the inactivation of ACh by blocking AChE

65
Q

􀁺 Cholinolytic drugs: drugs that inhibit ACh activity

A

􀁺 Muscarinic antagonists: M receptor antagonists
􀁺 Nicotinic antagonists: N receptor antagonists
􀁺 Drugs that speed the inactivation of ACh by activating AChE

66
Q

Common precautions for Cholinergic agonists . Why would cholinimimetics make things worse for these patients?

A

M3 agonism would exacerbate these conditions!

􀁺 Acute cardiac failure; bradycardia
-ACh slows HR 
􀁺 Asthma
-ACh causes vasoconstriction 
􀁺 Hyperthyroidism
-they increased sensitivity to catecholamines 
􀁺 Peptic ulcer
-ACh causes increased secretions 
􀁺 Urinary tract obstruction
􀁺 Parkinsonism
67
Q

Parkinsonism

A

-dysjunction between DA and ACh control in the basal ganglia
◦ decreased DA function
◦giving a cholinimimetic is like ACh running unrestrained and w/muscarinic receptor activation you can increase this

68
Q

Sjogren’s Syndrome

A

Chronic dry mouth due to autoantibodies against salivary glands

69
Q

Open vs Closed angle Glaucoma

A
  1. Open: Too much aqueous humor being produced
  2. Closed: Angle is small but production may be normal

Either condition , miosis (thus opening of the angle)
is beneficial

70
Q

Three Classes of AChE Inhibitors

A 
1. SImple Alcohols 
Quaternary amine
-they're simple competitive
inhibitors that drift in and
out over time
-Drug: edrophonium
  1. carbamic Acid Esters
    - covalently bonds but the bond is hydrolyzed water over time
    - Drugs: Neostigmine, Physostigmine
  2. Organophosphates
    - Covalently bonds and modifies AChE
71
Q

Organophosphates (Slide 87)

A

􀁺 “Irreversible” cholinesterase inhibitors covalently bind to AChE
􀁺 R groups may be alkyl, alkoxy, aryloxy, amido, and others
􀁺 X is the leaving group and can be halogen, cyano, thiocyanate, phenoxy, thiocholine, carboxylate, and others
􀁺 Uses: glaucoma, insecticides, nerve gases

72
Q

Mechanism/Effects of organophosphate

A

• permanent phosphorylation of the serine in AChE-only one drug can reverse this (pralidoxime)
• If not done within 24 hours (sooner the better) aging
will occur
◦ the R groups will form a covalent bond to other
parts of the enzyme’s active site and will no
longer be able to come back
◦ will need to make more enzyme (AChR) instead
◦ aging=irreversible inhibition

73
Q

Name two drugs that are antidotes for organophosphate poisoning:

A
  1. Atropine-muscarinic antagonist

2. pralidoxime-reversal of the poison binding to the AChE

74
Q

Ganglionic Antagonists

A
  1. 1st synapse thought the PNS (peripheral) is always a Nicotinic cholinergic synapse (nAChR)
  2. Ganglionic Antagonists block these 1st synapses
  3. They DO NOT block NMJ: cannot affect somatic movement
  4. Thus they can block all PSNS and SNS effects since they block the 1st synapse in PNS
75
Q

Effect of ganglionic blockade: General (Slide 104)

A
  1. Anything controlled by SNS will act like what it is under PSNS
  2. Vice versa for things under control of PSNS
76
Q

Effect of ganglionic blockade:

  1. arterioles
  2. veins
  3. Sweat Glands
A

***normally SNS

  1. Vasodilation, ↑ peripheral blood flow, hypotension
  2. Vasodilation, peripheral pooling of blood, ↓ venous return, ↓ cardiac output
  3. anhidrosis—need SNS stimulation to sweat
77
Q

Effect of ganglionic blockade:

  1. Heart
  2. Iris
  3. Ciliary Muscle
  4. GI Tract
  5. Urinary Bladder
  6. Salivary Glands
A

***normally PSNS

  1. Tachycardia
  2. mydriasis
  3. cycloplegia b/c normally ACh from PSNS causes the ciliary muscle to contract allowing tendons to relax and lens to bulge; now they’re just tonically relaxed by SNS
  4. ↓ tone and motility, constipation, ↓ gastric secretions
  5. xerostomia
78
Q

Effect of ganglionic blockade on HTN and HR

-Demonstrated w/a vasoconstrictor (slide 106)

A
  1. in HTN, normally baroreceptors will inhibit the SNS = HTN + brady
    * vagal tone
  2. However w/ganglionic blockade, you get HTN + unchanged HR or tachy: -because baroreceptors can no longer inhibit the SNS b/c they can’t communicate (no baroreceptor reflex)

Pharmacology (12 decks)

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