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Neuroscience > N27 - Autonomic pharmacology 2 > Flashcards

N27 - Autonomic pharmacology 2 Flashcards

1
Q

Give an overview of neurochemical transmission in the ANS.

A

1.Uptake of precursor
2. Synthesis of transmitter (T) or intermediate
3. Storage of transmitter (T) or intermediate
4. Depolarization by action potential
5. Ca2+ entry via voltage -activated Ca2+ channels
6. Ca2+ induced release of transmitter (exocytosis)
7. Receptor activation
8.Enzyme-mediated inactivation of transmitter (cholinergic)
OR
9. Reupatke of transmitter (adrenergic)

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2
Q

what are all these steps a target for?

A

drug target (often clinical significance)

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3
Q

What are the general features of cholinergic transmission.

A
  1. Uptake of choline via transporter (CHT). Rate limiting in synthesis of ACh
  2. Synthesis of ACh by choline acetyltransferase (ChAT). Acetyl coenzyme A (AcCoA) synthesised by mitochondria
  3. Storage of ACh within vesicle via transporter (VAChT). ATP and other anions are co-stored
  4. Depolarization of terminal by action potential
  5. Ca2+ influx through voltage-activated Ca2+ channels
  6. Ca2+- induced release of ACh from vesicles (exocytosis)
  7. Activation of ACh receptors (nicotinic, or muscarinic) causing cellular response
  8. Degradation of ACh to choline and acetate by acetylcholinesterase (AChE) – terminates transmission
  9. Reuptake and reuse of choline
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4
Q

what does the nicotinic acetylcholine (ACh) receptors consist of?

A

five glycoprotein subunits that form a central, cation conducting (Na+, K+ and Ca2+), channel

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5
Q

what is nicotinic acetylcholine receptors assembled from?

A

diverse range of subunits

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6
Q

what do nicotinic acetylcholine exist as?

A

numerous subtypes (dozens) that are structurally, functionally and pharmacologically distinct (4 well characterised subtypes)

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7
Q

what are the 4 subtypes?

A 
peripheral:
-skeletal muscle (alpha12bye)
-Ganglionic (alpha3b4)
CNS:
-alpha4b2
-alpha 7
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8
Q

what is the primary event?

A

cholinergic transmission at ganglia

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9
Q

what were drugs that block the autonomic ganglia once used for?

A

to control hypertension

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10
Q

what are the effects of autonomic ganglion blockade on tissues (site, predominant tone, effects of blockade)?

A
  • Arterioles -Sympathetic (adrenergic)-Vasodilatation; ↑ peripheral blood flow; hypotension
  • Veins- Sympathetic (adrenergic) -Vasodilatation; ↑ pooling of blood; ↓ venous return; ↓ cardiac output
  • Heart -Parasympathetic (cholinergic) - Tachycardia
  • Iris-Parasympathetic (cholinergic)-Mydriasis (pupil constriction)
  • Ciliary muscle -Parasympathetic (cholinergic) -Cycloplegia (focussed for far vision)
  • G.I. tract -Parasympathetic (cholinergic) -↓ Tone and motility; constipation; ↓ secretions
  • Urinary bladder -Parasympathetic (cholinergic) - Urinary retention
  • Salivary glands -Parasympathetic (cholinergic) -Xerostomia (dry mouth)
  • Sweat glands-Sympathetic (cholinergic)-Anhidrosis (absence of sweating)
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11
Q

what can blockade be achieved by?

A
  • depolarization block by high concentrations of agonists (e.g. nicotine)
  • competitive antagonism (e.g. trimetaphan)
  • Non-competitive antagonism
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12
Q

what is all ganglionic transmission (sympathetic and parasympathetic) selectively blocked by?

A

hexamethonium which illustrates an interesting molecular mechanism – open channel block – a form of non-competitive antagonism

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13
Q

Describe the stages of cholinergic transmission at parasympathetic neuroeffector junction?

A

Synthesis and storage of Each as previously described

  1. Depolarization by action potential
  2. Ca2+ influx through voltage-activated Ca2+ channels
  3. Ca2+- induced release of ACh (exocytosis)
  4. Activation of muscarinic ACh receptors subtypes (M1-M3) causing cellular response (tissue dependent)
  5. Degradation of ACh to choline and acetate by acetylcholinesterase (AChE) – terminates transmission
  6. Reuptake and reuse of choline
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14
Q

what is cholinergic transmission at parasympathetic neuroeffector junctions between?

A

varicosity of post ganglion neurone and effector cell. (e.g smooth muscle cell, gland cell)

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15
Q

what does M1 and Gq result in (G-Protein Coupled Muscarinic ACh Receptor Subtypes at Parasympathetic Neuroeffector Junctions)?

A
  • stimulation of phospholipase C

- increased acid secretion

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16
Q

what does M2 and Gi result in (G-Protein Coupled Muscarinic ACh Receptor Subtypes at Parasympathetic Neuroeffector Junctions)?

A
  • inhibition of adenylyl cyclase: opening of K channels

- decreased heart rate

17
Q

what does M3 and Gq result in (G-Protein Coupled Muscarinic ACh Receptor Subtypes at Parasympathetic Neuroeffector Junctions)?

A
  • stimulation of phospholipase C

- increased secretion (salivary)

18
Q

what is increased vascular smooth muscle indirectly relaxed by?

A

M3 receptor activation via NO

19
Q

What are the stages of noradrenergic transmission at sympathetic nueroeffector junctions?

A
  1. Synthesis of NA (multiple steps)
  2. Storage of NA by transporter (concentrates)
  3. Depolarization by action potential
  4. Ca2+ influx through voltage-activated Ca2+ channels
  5. Ca2+-induced release of NA
  6. Activation of adrenoceptor subtypes causing cellular response (tissue dependent)
  7. Reuptake of NA by transporters uptake 1 (U1) and uptake 2 (U2)
  8. Metabolism of NA by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)
20
Q

What is noradrenergic transmission at sympathetic nueroeffector junctions between?

A

Between nerve terminal of post-ganglionic neurone and effector cell (e.g cardiac and smooth muscle cell)

21
Q

what does B1 and Gs result in (G-Protein Coupled Adrenoceptor Subtypes at Sympathetic Neuroeffector Junctions)?

A
  • stimulation of adenylyl cyclase

- increased heart rate and force

22
Q

what does B2 and Gs result in (G-Protein Coupled Adrenoceptor Subtypes at Sympathetic Neuroeffector Junctions)?

A
  • stimulation of adenylyl cyclase

- relaxtation of bronchial and vascular smooth muscle

23
Q

what does alpha1 and Gq result in (G-Protein Coupled Adrenoceptor Subtypes at Sympathetic Neuroeffector Junctions)?

A
  • stimulation of phospholipase C

- contraction of vascular smooth muscle

24
Q

what does alpha2 and Gi result in (G-Protein Coupled Adrenoceptor Subtypes at Sympathetic Neuroeffector Junctions)?

A
  • inhibition of adenylyl cyclase

- inhibition of NA release

25
Q

what modulates the release of neurotransmitters?

A

presynaptic autoreceptors

26
Q

how does presynaptic auto receptor mediate negative feedback of transmitter release?

A

Agonists decrease release, antagonists increase release

27
Q

What is the effect of cocaine in the autonomic nervous system?

A
  • Cocaine Blocks U1 , increasing the concentration of NA in the synaptic cleft resulting in increased adrenoceptor stimulation
  • Peripheral actions cause vasoconstriction [alpha1 stimulation and cardiac arrhythmias [beeta 1 stimulation]
28
Q

What is the effect of amphetamine in the autonomic nervous system?

A
  • Amphetamine Is a substrate for U1 and enters the noradrenergic terminal where it inhibits MAO , enters the synaptic vesicle and displaces noradrenaline into the cytoplasm . Noradrenaline exits the terminal on U1 ‘running backwards’ and accumulates in the synaptic cleft causing increased adrenoceptor stimulation
  • Peripheral actions cause vasoconstriction (alpha1 stimulation) and cardiac arrhythmias (beta 1 stimulation)
29
Q

Describe the actions of prazosin in the autonomic nervous system.

A

Selective, competitive, antagonist of alpha 1. Does not block alpha2 ,beta 1 or beta 2 Vasodilator used as an anti-hypertensive agent

30
Q

Describe the actions of atenolol in the autonomic nervous system.

A

Selective, competitive, antagonist of beta 1. Does not block beta2,alph1 or alpha 2. Used as an anti-anginal and anti hypertensive agent

31
Q

Describe the actions of salbutamol in the autonomic nervous system.

A

Selective agonist at Beta 2. Does not activate beta1, alpha 1 or alpha 2. Used as a bronchodilator in asthma

32
Q

Describe the actions of atropine in the autonomic nervous system.

A

Competitive antagonist of muscarinic ACh receptors, does not block nicotinic ACh receptors. Blocks all muscarinic ACh receptors with equal affinity (1,2,3) - exerts widespread effects by blockade of the parasympathetic division of the ANS
(used to reverse bradycardia following MI and in anti cholinesterase poisoning )

Neuroscience (21 decks)

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