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Module 2D (Pt4) Flashcards

1
Q

What transmitters does adrenergic transmission consist of

A
  • Norepinephrine (NE)
    • Epinephrine
    • Dopamine
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2
Q

What is norepinephrine

A
  • Main transmitter of SNS post ganglionic gibers
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3
Q

What is epinephrine

A
  • The major hormone of the adrenal medula
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4
Q

What is dopamine

A
  • Main transmitter of other systems and pathways but we don’t learn them
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5
Q

What is the main neurotransmitter of the SNS

A
  • Norepinephrine
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6
Q

What are the different catecholamines

A
  • Norepinephrine
    - Epinephrine
    - dopamine
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7
Q

Catecholamines actions have therapeutic utility for what

A
  • Hypertension
    • Mental disorders
    • Bronchospasm
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8
Q

Catecholamines actions have therapeutic utility for what

A
  • Hypertension
    • Mental disorders
    • Bronchospasm
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9
Q

What are the parts of adrenergic transmission

A

i) Catecholamine synthesis
ii) Storage
iii) Release
iv) regulation
v) uptake
vi) Termination of release

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10
Q

Explain catecholamine synthesis

A

i) tyrosine is transported into the cell
ii) Tyrosine is converted to dopa by TH (tyrosine hydroxylase)
iii) DDOPA converted to dopamine by aromatic L- amino acid decarboxylase (AAADC)
iv) Dopamine transported into vescles by VMAT2
v) Dopamine converted to NE by Bopamine B- Hydroylase (DBH)
vi) NE converted to epinephrine by PNMT (phenylethanolamine-N-Methyl transferase in chromaffin cells of the adrenal medula

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11
Q

Is dopa the same as dopamine

A
  • No but DOPA is converted into dopamine
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12
Q

What enzyme converts DOPA into dopamine

A
  • Amino acid decarboxylase (AAADC)
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13
Q

What gets converted to DOPA by TH

A
  • Tyrosine
    • TH is tyrosine hydroxylase
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14
Q

What is the rate limiting step in catecholamine synthesis

A
  • Second step
    • Tyrosine is converted to dopa by TH (tyrosine hydroxylase)
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15
Q

Where is NE converted into epinephrine

A
  • In chromaffin cells of adrenal medula
    • Converted by PNMT
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16
Q

What are the parts of catecholamine storage

A

Uses Vesicular Monoamine transporter 2 (VMAT2)
i) Ph dependent pump
- Exchanges 2 H+ for one catecholamine

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17
Q

What inhibits VMAT2

A
  • Reserpine
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18
Q

What was reserpine historically used for

A
  • Hypertension, psychosis, dyskinesia in Huntington’s
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19
Q

Why is reserpine not used anymore

A

This is as it inhibits all VMAT2 as it is not specific

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20
Q

What does TH deficient humans have

A
  • Rigidity and hypokinesia
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21
Q

What does DBH deficiency cause in humans

A

Orthostatic hypotension

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22
Q

Catecholamine uptake

A
  • Mediated by Norepinephrine Transporter (NET)
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23
Q

What percent of NE will be uptaken or recycled and by what

A
  • About 87%
    • Recycled by NET
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24
Q

What is the Na+ dependent reuptake pump inhibited by and what occurs if it is

A
  • Tricyclic antidepressants (TCA) and cocaine
    • This makes NE (and other catecholamines) be help in the synaptic cleft where they can continue to do there job
    • Sympathetic nervous system on overdrive (super stimulated)
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25
What is the specificity of NET for the different catcholamines
- Dopamine > NE > epinephrine
26
What inhibits or reverses NET and VMATs and what does this mean
- Methamphetamines - This means that NET isn't only being blocked by it also pumps catecholamines into the synaptic cleft also so ever greater activation of SNS
27
Catecholamine release (release of NE)
- When an axon terminal depolarizes i) Voltage gates Ca channels open ii) Ca allows for interactions between VAMPs/ SNAPs and vesicles/ membranes iii) Membrane fusion occurs allowing NE to exit the cell by exocytosis
28
What are the SNAREs
- VAMPs and SNAPs
29
Is the release of NE the same process of Ach release
- Essentially yes
30
How does NE exit the cell
- Exocytosis
31
What happens when N-type Ca channels are inhibited
- Hypotension due to decreased NE
32
Regulation of NE release
- By autoreceptors
33
What is an autoreceptor
- A receptor present on the same cell as the released transmitter
34
What do a2A, a2B, a2C adrenergic receptors do
- Inhibit NE release - Through a negative feedback loop
35
What do B2 adrenergic receptors do
- Enhance NE release - Through a positive feedback loop
36
Termination of NE release
- Mediated by MAO (monoamine oxidase) and COMT (catechol-O-methyltransferase) When the NE is taken up MAO and COMT go to work
37
Difference between MAO and COMT
- COMT is not associated within the SNS - Sympathetic nerves have MAO but not COMT
38
What do MAO and COMT do
- Stop the release of NE
39
What are inhibitors of MAO and CMT useful for
- CNS effects (depression, parkinsons) - Have few peripheral effects
40
True of false: cocaine is a stimulant of the SNS
- True - Cocaine inhibits NET, so keeps the NE in the synaptic cleft so is a stimulant, this causes the SNS to be exacerbated
41
What do a receptors do
- Alpha - Smooth muscle cells of organs and blood vessels around organs - NE binds and causes contriction which means less blood flow
42
What do B receptors do
- Beta - Heart and blood vessels around lung and muscle - NE binds and causes relaxation meaning more blood flow
43
What are the Gq coupled GPCRs
a1A,B,D
44
What do Gq- coupled GPCRs do
- Activates the G protein, calcium release and contraction
45
What are the Gi- coupled receptors
- A 2A,B,C
46
What do the Gi coupled GPCRs do
- I= inhibit - ATP decreases, K channels activated, Ca channels inhibited - Causes hyperpolarization
47
What are the Gs coupled GPCRs
- B1,2,3
48
What do the Gs- coupled GPCRs do
- Stimulate; opposite of gi - Camp increases, K channels inhibited, Ca channels activated - Increase in excitability and contraction - Present in heart and blood vessels of lungs
49
Other names for desensitization
- Refractoriness - Tachyphylaxis
50
What is Desensitization
- a progressive diminished response due to repeated exposure of catecholamine sensitive tissue to agonists
51
What are the causes of desensitization
- GRKs (G protein receptor kinases) - Barrestins - Receptor sequestration - Endocytosis
52
When desensitization occurs what do you need to do with drug dosing
- Need a larger dose of the drug to cause the same response - Can cause more adverse effects
53
If you have a drug that was an agonist (causes a response)of beta receptors what is the effect on the heart
- Contraction, force and heart rate will go up
54
What are sympathomimetics
- Adrenergic agonists
55
What are organ effects from sympathomimetics (eye, lung, Genitourinary tract, vascular system, Heart, metabolic)
i) Eye - Decrease intraocular pressure through mydriasis (a1 agonists: phenylephrine) - Decrease intraocular pressure through aqueous humor (a2 agonists) ii) Lung - can treat bronchospasm (asthma) through B2 agonists (isoproterenol, albuterol) iii) Genitourinary tract - Increase sphincter tone in bladder through a1 agonists iv) Vascular system - Increase blood pressure through reflex bradycardia (a1 agonists) - Increase bp i.v. or topically (a2 agonists: clonidine) - Decrease bp in skeletel muscle arterioles (B2 agonists) v) Heart (B1, B2 receptors) - Increase cardiac pacemaker rate - Increase atrioventricular node conduction - Increase cardiac force vi) Metabolic - Increase renin secretion (B1 agonists) - Increase insulin secretion, glycogenolysis (in liver) (B2 agonists)
56
What is the baroreceptor reflex
- A homeostatic response to maintain blood pressure through sensing pressure changes and response to change in tension of the arterial wall
57
Steps of the baroreceptor reflex
i) NE: a and B agonist ii) A increase blood pressure and B increase Heart rate iii) The increase bp triggers the vagus nerve which then decreases heart rate (vagal reflex arc)
58
What is the difference between specific and non specific agonists (NE vs isoproterenol)
i) NE - Agonist of a and B receptors - Cause an increase in both systolic and diastolic BP - The a increases blood pressure (constrict certain blood vessels) - The B increase Heart rate - The increase in BP triggers the Vagus nerve and this decreases heart rate ( Vagal reflex arc) - This means get an increase in bp and decrease in heart rate ii) Isoproterenol - Selective with B receptors - Causes a huge increase in heart rate but the bp only briefly goes up but then goes down as the a receptors arent being activated
59
What is isoproterenol and what does it do
- A B1,2 agonist - Increase heart rate and decrease bp by vasodilation in skeletal muscle
60
Adrenergic agonist clinical utility
1. Anaphylaxis - Hypotension, bronchospasm, angioedema - Example: epinephrine 2. Allergy and glaucoma - Itching, miosis, Intra ocular pressure - Example: phenylephrine (a), brimonidine (a2) 3. Acuta astham - Bronchospasm and constriction - Example: albuterol (B2) 4. Heart failure and shock - Increase blood flow - NE 5. Decongestant - Decrease blood flow - Phenylephrine, ephedrine (a) 6. Cardiac stimulation and AV block - Epinephrine 7. urinary incontinence - Ephedrine
61
Do selective agonists bind to other receptors
- Yes nothing is perfectly selective - At high enough dose there will be non specific side effects - B1: can cause tachycardia, arrhythmia - a1: hypertension - B2: skeletal muscle tremor
62
Adrenergic antagonist utility
- Anywhere we want to block the SNS activity i) Non selective B - Acute angle closure glaucoma (timolol), local anesthetics and anxiety ii) B1 - Hypertension, angina, arrhythmia, heart failure iii) Nonselective a - Pheochromocytoma iv) a1 - Usually end in osin - Hypertension, urinary retention v) a2 - Reversal of sedation
63
What do B adrenergic antagonists usually end in
- Olol
64
What causes adrenergic antagonist toxicity
- A natural extension of their pharmacological actions
65
What happens when we use adrenergic antagonists
- If we block the SNS we allow the PNS to go up
66
Examples of adrenergic antagonist toxicity
- Bradycardia - Atrioventricular blockade - Heart failure - Asthma attacks - Sexual dysfunction
67
What does it mean when B-blockers start with a-m (excluding c)
They are B1 selective

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