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Principles 2018 > Pharmacology Part 7 > Flashcards

Pharmacology Part 7 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, or intermediate
  4. Depolarisation 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. Reuptake of transmitter (adrenergic)
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2
Q

Give an overview of cholinergic transmissio?

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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3
Q

Describe the structure of nicotinic acetylcholine receptors

A

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

> Can be assembled from a diverse range of subunits (a1-10, B1-4, y, epsilon, delta)

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4
Q

What are the four well characterised ACh receptor subtypes?

A

Peripheral
>Skeletal muscle (a1)2Bgammaepsilon

> ganglionic
a3B4

CNS
>a4B2
>a7

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5
Q

What is (cholinergic) excitatory transmission at ganglia caused by

A

ACh released from preganglionic neurones that activate cation-selective nicotinic receptors of the postganglionic neurone cell body to elicit the rapid excitatory postsynaptic potential

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6
Q

What happens to postganglionic neurones in absence of excitatory synaptic input?

A

Silent

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7
Q

What are most postganglionic neurones innervated by?

A

sympathetic and parasympathetic are innervated by several presynaptic fibres

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8
Q

Is esps from one preganglionic input significant enough to trigger an action potential?

A

Yes but more generally simultaneous activity of several inputs is required

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9
Q

What do postganglionic and preganglionic fibres have in common?

A

utilize transmitters (e.g. peptides) other than ACh that may modulate ganglionic transmission

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10
Q

What is the predominant tome of the arterioles?

A

Sympathetic (adrenergic)

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11
Q

What is the predominant tone of the veins?

A

Sympathetic (adrenergic)

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12
Q

What is the predominant tone of the heart?

A

Parasympathetic (cholinergic)

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13
Q

What is the predominant tone of the iris, ciliary muscle, gi tract, unrinaty bladder and salivary glands?

A

Parasympathetic (cholinergic)

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14
Q

What is the predominant tone of the sweat glands?

A

Sympathetic (cholinergic)

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15
Q

How is blockade of cholinergic transmission at ganglia achieved?

A

> depolarization block by high concentrations of agonists (e.g. nicotine)
competitive antagonism (e.g. trimetaphan)
Non-competitive antagonism

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16
Q

What does hexamethonium do?

A

Blocks all ganglionic transmission (open channel block)

17
Q

How does cholinergic transmission at parasympathetic neuro-effector junctions occur?

A
  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 receptor 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
18
Q

What does M1 GPCR couple with, stimulate and cause?

A

Gq
Phospholipase C
Increased acid secretion

19
Q

What does M2 GPCR couple with, inhibit and cause?

A

Gi
Inhibition of adenylyl cyclase
Opening of K+ channels
Decreased Heart rate

20
Q

What does M3 GPCR couple with, stimulate and cause?

A

Gq
Phospholipase C
Increased saliva secretion
Contraction of visceral and relaxation of vascular smooth muscle

21
Q

Describe noradrenergic transmission at sympathetic neuroeffector 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)
22
Q

What branch of the nervous system are M cholinergic receptors?

A

Parasympathetic

23
Q

What does B1 GPCR couple with, stimulate and cause?

A

Gs
Adenylyl cyclase
Increased HR and force

24
Q

What does B2 GPCR couple with, stimulate and cause?

A

Gs
Adenylyl cyclase
Relaxation of bronchial and vascular smooth muscle

25
Q

What does a1 GPCR couple with, stimulate and cause?

A

Gq
Phospholipase C
Contraction of vascular smooth muscle

26
Q

What does a2 GPCR couple with, inhibit and cause?

A

Gi
Adenylyl cyclase
Inhibition of NA release

27
Q

What do presynaptic auto receptors mediate?

A

Negative feedback inhibition of transmitter release.
Agonists: decrease release
Antagonists: increase release

28
Q

Describe the function of cocaine?

A

Blocks U1, increasing the concentration of NA in the synaptic cleft resulting in increased adrenoceptor stimulation

29
Q

What are the peripheral actions of cocaine?

A

actions cause vasoconstriction [a1 stimulation] and cardiac arrhythmias [B1 stimulation]

30
Q

Describe the action of amphetamine?

A

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

31
Q

What are the peripheral actions of amphetamine

A

Largely the same as cocaine

32
Q

Describe the action of prazosin?

A

Selective, competitive, antagonist of a1. Does not block a2, B1, or B2. Vasodilator used as an anti-hypertensive agent

33
Q

Describe the action of atenolol

A

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

34
Q

Describe the action of salbutamol?

A

Selective agonist at B2. Does not activate, B1, a1, or a2. Used as a bronchodilator in asthma

35
Q

Describe the action of atropine?

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

36
Q

What is atropine used for?

A

reverse bradycardia following MI and in anticholinesterase poisioning

Principles 2018 (34 decks)

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