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Pharmacology > Autonomic Nervous System: Cholinergic and Adrenergic Agents > Flashcards

Autonomic Nervous System: Cholinergic and Adrenergic Agents Flashcards

1
Q

Mecamylamine

A

A ganglionic blocking drug of both parasympathetic and sympathetic (Nn) receptors.

Used as an antihypertensive drug (peripheral vasodilator) and tobacco smoking cessation (blocks Nn receptors in reward center of brain).

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2
Q

What is the rate-limiting step of Ach synthesis?

A

The transport of choline into the pre-synaptic nerve endings by Na+-choline co-transporter

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3
Q

Steps of Ach synthesis

A
  1. Choline transported into pre-synaptic nerve endings by Na+-choline co-transporter
  2. Choline + Acetyl CoA–> Ach by a cytosolic choline acetyltransferase (ChAT)
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4
Q

Ach storage

A

In the nerve terminal vesicles

Active vesicular uptake by a H-Ach antiporter, Ach is ion trapped (+charged) in the vesicle

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5
Q

Ach Release

A

AP–> Ca influx –> docking of vesicle with plasma membrane –> release of Ach by exocytosis – Ach is always charged and therefore can’t cross membranes

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6
Q

Presynaptic Inhibition of Cholinergic Transmission is done by _______.

A

Botulinum toxin (deadly nightshade) - prevents the release of Ach

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7
Q

Hemicholinium

A

Prevents choline from entering the pre-synaptic nerve ending

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8
Q

Vesamicol

A

Prevents the storage of Ach into vesicles

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9
Q

onabotulinumtoxinA (Botox)

Mechanism

A

PRE SYNAPTIC DRUG

Mechanism: inactivates SNAP-25 required for docking of the vesicle with the presynaptic membrane

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10
Q

onabotulinumtoxin A (Theraputic uses)

A
  1. Muscle spasms/dystonias (strabismus aka lazy eye–inject into dominant eye), blepharospasm (eyelid muscle spasm that shuts eyelids)
  2. Cosmetic - reduce glabellar, forehead, and lateral canthus lines, given IM
  3. Axillary hyperhidrosis (prevent sweating) - intradermal
  4. Chronic migraines, IM
  5. Overactive bladder disorder, intra-detrusor muscle
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11
Q

Onabotulinumtoxin A (side effects)

A
  1. Dysphagia and breathing difficulties (boxed warning) - from distant spread beyond injection site
  2. Muscle weakness (ptosis), urinary retention, pain
  3. Allergic reaction (due to it being a protein coming from a foreign bacteria)
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12
Q

Onabotulinumtoxin A (drug action)

A

Drug action: flaccid paralysis of skeletal muscle softens facial wrinkles and relaxes muscle spasms; inactivates sweat glands

Restoration of function requires sprouting of new nerve terminals; duration 3-4 months (irreversible inactivation)

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13
Q

Cholinergic Receptor Subtypes

A

Muscarinic: GPCRs
Nictonic

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14
Q

M3

A

(Smooth muscle, gland, endothelium)
Mediates excitation/contraction/secretion

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15
Q

M2

A

(heart) - Gi –> signals cellular inhibition

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16
Q

Muscarine

A

PRE-SYNAPTIC DRUG

Prototype AGonist of Botulin Toxin; activates all M subtypes

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17
Q

Atropine

A

PRE SYNAPTIC DRUG

Prototype ANTAGonist of Botulism Toxin: blocks M subtypes

Sits on receptor to block but activates opposing response due to blocking

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18
Q

Nicotinic Receptors

A

Ligated ion channels with a fast response time

Stimulation increases permeability to Na+ causing membrane depolarization; persistent stimulation causes destimulation of receptor

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19
Q

Nn

A
  • neuronal (ganglia, adrenal medulla-Epi)
  • high-affinity agonist - Nicotine (stimulation followed by desensitization)
  • Prototype antagonist - Mecamylamine (anti-hypertensive agent)
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20
Q

Nm

A

-musculoskeletal; NMJ
- low-affinity agonist - Nicotine (stimulating –> densensitized –> skeletal muscle paralysis)
-prototype antagonist - d-tubocurarine (produces non-depolarizing (competitive) neuromuscular blockade

21
Q

Nicotine

A

PRE SYNAPTIC DRUG

High affinity agonist to Nn, low affinity agonist to Nm

Can look like an antagonist due to how tightly it binds

22
Q

d-tubocurarine

A

PRE SYNAPTIC DRUG

A prototype ANTAGonist for Nm that produces a depolarizing (competitive) neuromuscular blockade

23
Q

Acetylcholinesterase (AChE)

A

rapidly terminates cholinergic NT by hydrolysis of ACh

24
Q

Butyrylcholinesterase (BuChE)

A

expressed mainly in the plasma and liver. Is a drug-metabolizing enzyme of choline ester drugs (ACh). – only does Ach when injected –

25
Steps for synthesis of Catecholamines - DA, NE, Epi
Tyrosine --(Tyrosine hydroxylase)--> Dopa -- (LAAAD)--> Dopamine --(Dopamine beta hydroxylase) --> NE --(PNMT)--> Epi Tyrosine --> Dopa is the rate-limiting step
26
CNS basal ganglia and renal vasculature release...
Dopamine
27
Adrenergic neurons release...
Norepinephrine
28
Adrenal medulla releases...
Epinephrine because it has all four converting enzymes to convert NEpi--> Epi
29
The release of cortisol in the cortex stimulates ______ and ______ release in the adrenal medulla.
Epi and NE
30
Monoamine oxidase (MAO)
- Degrades any catecholamine molecule that isn't stored - In sympathetic nerve terminals, liver, and brain - Two isoforms: A , B; degrade tyramine (A), and histamine (B) -
31
Vesicular Monoamine Transporter (VMAT-2)
Actively transports catecholamines into vesicles -- which are then passively diffused out of the storage vesicles
32
Reserpine (Mechanism)
Inhibits VMAT-2 thus depleting catecholamines from being stored in vesicles and reduces CNS sympathetic outflow (Dopamine)
33
Reserpine (therapeutic use)
Used as an old hypertensive: caused sedation, psychotic depression, and orthostatic hypotension
34
Release of catecholamines
Same process as with cholinergic neurons (AP, Ca2+ influx, exocytosis)
35
alpha-2 auto-receptors
Stimulation causes negative feedback inhibition of NE release -- Gi inhibition of Ca2+ influx
36
Antagonists of alpha-2 auto-receptors do what
Increase NE release
37
Tyramine
PRE SYNAPTIC DRUG Toxic amino acid in food (aged cheese, beer/wine, cured meat) that stimulates NE release -- can cause hypertensive crisis by increasing sympathetic nerve terminal activity at heart and vasculature
38
Tyramine (Mechanism)
Displaces NE from storage vesicles; elevated cytosolic NE triggers non-vesicular release by reverse transport through NET
39
(Norepinephrine Transporter) NET
An intra-membranous transporter that can transport NE in either direction
40
Why would a patient be at risk if they are on an MAOI (Monoamine Oxidase Inhibitor) and they consume Tyramine?
MAO degrades unstored NE and a MAOI will inhibit MAO from degrading free NE. Since tyramine displaces NE from storage vesicles, without MAO, NE will cause a hypertensive crisis. --- therefore patient's on MAOIs must have dietary restrictions
41
Methyldopa (Therapeutic)
Gestational hypertension (safe for developing fetus) -- side effects are dry mouth, edema, elevated risk of autoimmune hemolytic anemia (+Coombs' test) with long-term use
42
Methyldopa (Mechanism)
PRE SYNAPTIC DRUG Alpha-2 agonist prodrug converted by DOPA decarboxylase --> methyl-dopamine and then by dopamine beta-hydroxylase --> methyl-NE (active form). - Methyl-NE binds to alpha-2 to halt release of NE. Inhibits NE release and thus lowers blood pressure by decreasing sympathetic outflow from CNS to the heart, vasculature, and kidneys
43
Adrenergic Receptor Subtypes
All coupled to G-proteins (GPCRs) Pre-synaptic: alpha 2 - Gi: decrease cAMP, M2 receptor in heart to slow HR Postsynaptic: alpha 1 - Gq: M3 receptor for vasoconstriction beta 1 - Gs: increases cAMP; excitatory/contraction beta 2 - Gs: relaxation of smooth muscle beta 3 - Gs: relaxation of smooth muscle, lipolysis
44
Cocaine
-PRE-SYNAPTIC DRUG blocks reuptake of NE from NET. - a local anesthetic for pain similar to lidocaine, novocaine etc. -- but only one to block reuptake of NE -- thus NE continuously fires in NMJ
45
What are MAOIs used for therapeutically?
Depression and Parkinson's disease
46
Catechol-O-methyltansferase (COMT)
- In the liver and kidney - Methylates and clears catecholamines (metabolism) - COMT inhibitors are used for Parkinson's disease
47
Both MAO and COMT do what?
They both metabolize NE and result in the production of VMA
48
VMA
- End results from metabolism of NE by COMT and MAO. - Major metabolite excreted in the urine; basis of clinical tests for pheochromocytoma (tumor of the adrenal medulla) - elevated in a hypertensive crisis when sympathetic nervous system is over activated
49
Cholinergic Agonists and Antagonists
Agonists: "A big python came" Acetylcholine (prototype) - Bethanechol, pilocarpine, cevimeline Antagonists: "And snuck by two Irish toddlers" Atropine (prototype) - scopolamine, ipratropium bromide, tolterodine, tropicamide

Pharmacology (2 decks)

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