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Pharmacology > The Autonomic Nervous System > Flashcards

The Autonomic Nervous System Flashcards

1
Q

what are the two large divisions of the autonomic nervous system?

A

sympathetic and parasympathetic

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2
Q

what do the sympathetic and parasympathetic nervous systems do?

A

provide link between the central nervous system and peripheral organs. involuntary systems.

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3
Q

what is the basic anatomy of the autonomic nervous system? (which parts?)

A

cervical, gastrointestinal, lumbar, medullary, sacral, thoracic.

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4
Q

basic sections of sympathetic nerves?

A

thoracic, lumbar sections of spinal cord.

preganglionic nerves - ganglion - post ganglionic nerve.

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5
Q

basic sections of parasympathetic nerves?

A

cranial, sacral sections of spinal cord.

Preganglionic nerves – ganglion – postganglionic nerve.

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6
Q

basic difference between sympathetic and parasympathetic nerves?

A

s: preganglionic nerves short. ganglion located outside of innervated tissue

p: preganglionic nerves long. ganglion located within innervated tissue

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7
Q

name two neurotransmitters of the autonomic nervous system:

A

acetylcholine, noradrenaline.

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8
Q

noradrenergic neurons: what does it do and where is it located?

A

synthesize noradrenaline. located in periphery are sympathetic neurons, whose cell bodies lie in sympathetic ganglia.

store noradrenaline in vesicles and release into synaptic cleft. re-uptake of noradrenaline from synaptic cleft by noradrenaline transporter (SLC6A2) to reduce its effect

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9
Q

within the autonomic nervous system, what are cholinergic neurons?

A

choline taken up into the nerve. free choline within the nerve terminal is acetylated by choline acetyltransferase (CAT), which transfers the acetyl group from acetyl coenzyme A.

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10
Q

what terminates the effect of released acetylcholine?

A

acetylcholinesterase (AChE)

ACh + AChE –> choline and acetate.

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11
Q

what does botulinum toxin do?

A

Inhibits acetylcholine release from cholinergic neurons –> prevent exocytosis. progressive parasympathetic and motor paralysis.

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12
Q

name two indications of botulinum toxin poisoning

A

blepharospasm (persistent eyelid spasm)
urinary incontinence.

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13
Q

Anticholinesterease drugs: effects?

A

Inhibit acetylcholinesterase.
increases acetylcholine concentration by preventing its metabolism

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14
Q

Anticholinesterease drugs: effects mainly due to?

A

enhancement of cholinergic transmission at cholinergic autonomic synapses (and neuromuscular junction)

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15
Q

examples of anticholinesterease drugs: short acting and medium duration?

A

short: edrophonium
medium: neostigmine

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16
Q

indications of anticholinesterase drugs?

A

myasthenia gravis

(antibodies destroy the communication between nerves and muscle, resulting in weakness of the skeletal muscles. affects voluntary muscles)

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17
Q

simply: what are agonists and receptors of the following: pre-ganglionic nerves, sympathetic nerves, parasympathetic nerves.

A
  1. acetylcholine –> nicotinic receptors
  2. noradrenaline –> adrenoceptors
  3. acetylcholine –> muscarinic receptors
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18
Q

what releases adrenaline into vascular system to activate adrenoceptors?

A

adrenal medulla

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19
Q

what are nicotinic receptors activated by?

A

acetylcholine released from pre-ganglionic nerves

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20
Q

what happens when nicotinic receptors are activated?

A

tachycardia, an increase in blood pressure, and variable effects on gastrointestinal motility and secretions. salivary and sweat secretions

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21
Q

what are nicotinic receptors blocked by?

A

hexamethonium –> transmission block. causes hypotension and loss of cardiovascular reflexes (prev used to manage hypertension. ‘hexamethonium man’)

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22
Q

Name an exogenous agonist that activates nicotinic receptors. (what does exogenous agonist mean?)

A

Nicotine

external factors which bind to various receptors. induce biological response.

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23
Q

classification of adrenoceptors? (name first three)

A

alpha1, alpha2, beta. each splits into three further groups.

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24
Q

noradrenaline: where is it released, what does it activate?

A

released from sympathetic nerve terminals activates adrenoceptors

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25
Q

activation of a1 adrenoceptor: main effect?

A

vasoconstriction, gastrointestinal smooth muscle relaxation, salivary secretion, hepatic glycogenolysis

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26
Q

activation of a2 adrenoceptor: main effect?

A

inhibition of transmitter release (noradrenaline and acetylcholine release from autonomic nerves), platelet aggregation, contraction of vascular smooth muscle, insulin release inhibition.

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27
Q

activation of b1 adrenoceptor: main effect?

A

increased cardiac rate and force. delayed cardiac hypertrophy

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28
Q

activation of b2 adrenoceptor: main effect?

A

bronchodilation, vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis, muscle tremor

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29
Q

activation of b3 adrenoceptor: main effect?

A

lipolysis.

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30
Q

can adrenoceptors co-exist? give example and effect.

A

b1 and b2 adrenoceptors in human heart. increase heart rate and force of contraction.

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31
Q

what family do the adrenoceptors/muscarinic receptors belong to?

A

G-protein coupled receptors. (GCPRs)

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32
Q

beta1 adrenoceptor: binding pocket: what does GPCR do?

A

GPCRs form a ‘binding pocket’ where agonists and antagonists enter.
agonists and antagonists bind to specific amino-acids on the GPCR

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33
Q

What does G-protein-coupled receptor (GPCR) act like in the cell? What is the role of the binding pocket in the GPCR?

A

GPCR receives signals from the outside. The binding pocket is where the receptor grabs onto specific molecules.

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34
Q

What is the function of agonists in GPCR signaling?

A

Agonists, like adrenaline, stabilize the receptor in a way that activates it and couples it to the cell’s internal G-protein, triggering a response.

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35
Q

How do antagonists, such as cyanopindolol, affect GPCR signaling?

A

Antagonists stabilize the receptor differently, preventing it from coupling to the G-protein and stopping the signal.

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36
Q

What happens to the pocket around adrenaline in GPCR binding?

A

There is a 2–3A ° tightening of the pocket around adrenaline, ensuring a strong and clear signal. (antagonists don’t produce this response)

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37
Q

critical anchoring points (endogenous catecholamines): when is beta2 adrenoceptor activated most effectively?

A

when there are precisely 2 carbon atoms between the ring and the amino group.

catecholamines: (class of neurotransmitter/hormone. e.g. dopamine, noradrenaline, adrenaline). endogenous means produced naturally in the body.

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38
Q

what is the neurotransmitter released from sympathetic nerve terminals and activates adrenoceptors?

A

noradrenaline

39
Q

neurotransmitter released from parasympathetic nerve terminals and activates muscarinic receptors:

A

acetylcholine

40
Q

neurotransmitter released from pre-ganglionic receptors and activates nicotinic receptors:

A

acetylcholine

41
Q

neurotransmitter that is a substrate for SLC6A2

A

noradrenaline

42
Q

neurotransmitter synthesized from dopamine by dopamine beta-hydroxylase:

A

noradrenaline

43
Q

give three examples of catecholamines:

A

noradrenaline, adrenaline, isoprenaline.

44
Q

What are the structural features studied in β1- and β2-adrenoceptors?

A

structural features: for example, interaction with protonated amine group.

45
Q

What is the role of the amine group in β-blockers like propranolol in interacting with the β2-adrenoceptor?

A

works as an anchor.

The amine group of β-blockers like propranolol anchors these compounds to the Asp113 in the β2-adrenoceptor.

46
Q

what structural substitution results in reduction of agonist activity?

A

Tertiary amine substitution ex –
N(CH3)2 - reduces agonist activity

47
Q

name three full agonists of β1AR, β2AR

A

noradrenaline, adrenaline, isoprenaline.

48
Q

nicotinic receptors are activated by? where is it released?

A

activated by acetylcholine released from pre-ganglionic nerves.

49
Q

what are indirect acting sympathomimetic drugs? what are their classifications? (4)

A

enter sympathetic nerve terminals and displace noradrenaline from storage vesicles.

phenoethylamines
phenylethanolamines
phenylethylamines
aliphatic amines

50
Q

indirect acting sympathomimetic drugs: phenoethylamines: give function and example.

A

tyramine: acts almost entirely by displacing noradrenaline from stores in sympathetic nerve terminals.

51
Q

indirect acting sympathomimetic drugs: phenylethanolamines: give function and example.

A

ephedrine: has four isomers. have largely indirect action. ephedrine isomers with same configuration about beta-carbon as noradrenaline have more direct activity on beta adrenoceptors.

52
Q

indirect acting sympathomimetic drugs: phenylethylamines: example, characteristics and activity?

A

amphetamine, methylamphetamine. taken up into sympathetic nerve terminal. cause displacement of noradrenaline from storage vesicles. have alpha-chiral carbon.

absence of meta- and para-hydroxyl and beta hydroxyl groups reduce direct beta adrenoceptor activity.

53
Q

example of partial agonist? + structure.

A

dobutamine: absence of beta hydroxyl and inclusion of bulky N-substitution cause reduction in efficacy at beta adrenoceptors.

dobutamine has chiral carbon.

54
Q

what does propranolol do? (effects on the body)

A

decrease heart oxygen demand by blocking beta receptors, decrease heart workload. manage coronary artery disease.

55
Q

properties of beta blockers: competitiveness?

A

all beta blockers are competitive antagonists.

56
Q

Name the categories of β-blockers based on selectivity.

A

Non-selective β-blockers (First generation)

Selective β-blockers (Second generation)

β-blockers with vasodilatory effects (Third generation)

57
Q

Give an example of a β-blocker with intrinsic sympathomimetic activity (ISA).

A

Oxprenolol (partial agonist)

58
Q

Provide examples of β-blockers with inverse agonist activity.

A

Metoprolol, Nadolol (though not used in Australia)

59
Q

What structural feature in propranolol results in a loss of agonist activity at β-adrenoceptors?

A

–O-CH2- bridge between the aromatic ring and β-hydroxyl carbon and absence of meta- and para-hydroxyl groups on the aromatic ring.

60
Q

What structural features do all clinically used β-blockers share?

A

–O-CH2- bridge and lack meta- and para-hydroxyl groups.

61
Q

what drug are beta1 selective blockers based on? what are the significant structural aspects? give some examples of blockers.

A

isoprenaline (synthetic catecholamine)

-O-CH2- oxymethylene group
- para aromatic ring substitution
- absence of a meta aromatic ring substitution

ex. atenolol, metoprolol, bisoprolol.

62
Q

beta adrenoceptor antagonists with vasodilatory activity: example, what does it block and why, and effect.

A

carvedilol.

blockade of alpha1 adrenoceptors –> relax smooth muscle.

highly lipophilic –> persistent blockade of beta-adrenoceptors.

63
Q

beta adrenoceptor antagonists: beta blockers. therapeutic indications and examples?

A
  • hypertension (metoprolol, atenolol)
  • coronary artery disease (metoprolol, atenolol)
  • heart failure (metoprolol, carvedilol, bisoprolol, nebivolol)
  • arrhythmias (atenolol, esmolol) (sometimes sotalol, but also potassium ion channel blocker)
64
Q

the endogenous agonists for alpha1 adrenoceptors are?

A

noradrenaline and adrenaline.

65
Q

What structural feature characterizes drugs like phenylephrine and metaraminol in activating alpha-1 adrenoceptors?

A

characterized by a meta-hydroxyl or a meta-substituent on the aromatic ring.

66
Q

What is the effect of activating alpha-1 adrenoceptors?

A

vasoconstriction.

67
Q

Name two drugs that activate alpha-1 adrenoceptors and have a meta-hydroxyl.

A

Phenylephrine and metaraminol

68
Q

What is the primary action of imidazolines on adrenoceptors?

A

direct agonists on α1A adrenoceptors

69
Q

Why do most imidazoline compounds have poor intrinsic activity?

A

due to different binding patterns compared with noradrenaline. additionally, most do not have chiral centres.

70
Q

For what purpose are imidazolines commonly used?

A

‘nasal ‘decongestants.’

71
Q

alpha 1 adrenoceptor: selective antagonist. give two examples:

A

prazosin, terazosin.

72
Q

nature of alpha2 adrenoceptors? what does it do?

A

Pre-junctional alpha2-adrenoceptors are autoinhibitory

-reduce the amount of (-)-noradrenaline released from sympathetic nerve terminals

73
Q

location of the following? (cardiovascular control)(pre/post junctional and effects?)
beta1 adrenoceptor, beta2 adrenoceptor, alpha2 adrenoceptor.

A

beta1 adrenoceptor: postjunctional (increase force of heart contraction and heart rate)

beta2 adrenoceptor: prejunctional (increase noradrenaline release), postjunctional (decrease vascular tone)

alpha2 adrenoceptor: prejunctional (decrease noradrenaline release)

74
Q

mechanism of imidazoline antihypertensive drugs? function and effect.

A

reduce release of sympathetic transmitter (noradrenaline).

decrease vascular resistance, heart rate, force of contraction.

75
Q

five members of muscarinic receptors and G protein coupling?

A

Five members, M1, M2, M3, M4, M5
- G-protein coupled receptors
- M2, M4 coupled to Gi/Go proteins
- M1, M3, M5 coupled to Gq/11 proteins

76
Q

types of muscarinic receptors and type (e.g. cardiac)

A

M1 = neural
M2 = cardiac
M3 = glandular
M4, M5 = molecular mAChR subtypes. mainly occur in CNS

77
Q

muscarinic receptor agonists: example

A

acetylcholine. hydrolysed by cholinesterase. effect of muscarinic receptor agonists mimic the effects of acetylcholine.

78
Q

muscarinic receptors: agonists: effects on the heart.

A

decreased heart rate, force of atrial contraction, force of ventricular contraction.

79
Q

muscarinic receptors: agonists: effects on the blood vessels.

A

relaxation: endothelium dependent. NO mediated.

contraction: smooth muscle dependent.

80
Q

muscarinic receptors: agonists: effects on the smooth muscle, sweating, lacrimation, salivation and bronchial secretion:

A

contraction: ^peristaltic activity in gastrointestinal tract, bronchial constriction.

increase secretions

81
Q

muscarinic receptors: agonists: effects on acid release from parietal cells in gastrointestinal system:

A

increased acid release –> decrease pH of stomach lumen.

82
Q

muscarinic receptors: agonists: effects on the the eye and example of drug? what is it used to treat?

A

constrictor pupillae muscle –> constrict pupil. lowers IOP in patients with glaucoma.

pilocarpine eye drops used for glaucoma.

ciliary body contraction –> lens bulges more induce decrease focal length.

83
Q

what structural change occurs when M2 receptor is activated?

A

transmembrane helix 6 (TM6) rotates outward, Tm7 moves inward. G-protein binding site formed intracellularly.

84
Q

types of muscarinic receptor antagonists. give example of each.

A

1 irreversible muscarinic receptor antagonist: phenoxybenzamine

2 reversible (competitive receptor antagonists): atropine.

85
Q

muscarinic receptors: antagonists: effects on the heart, gastrointestinal tract smooth muscle

A

increase heart rate

decrease motility and acid release (more basic)

86
Q

muscarinic receptors: antagonists: effects on other smooth muscles and secretions. (effects on eye the opposite of agonist)

A

bronchial, biliary and urinary tract smooth muscle relaxation

decrease salivary, lacrimal, bronchial and sweat glands –> dry mouth and skin.
decrease acid release from parietal cells (increase pH of stomach lumen (gastrointestinal))

87
Q

what type of drug is atropine?

A

muscarinic receptor antagonist.
peripheral indications (meaning apart from primary use): bradyarrhythmia.

88
Q

selectivity of muscarinic receptor antagonists?

A

relative lack of selectivity for individual receptors.

“development of drugs of other clinical applications held back possibly due to lack of small molecule ligands that can inhibit/activate specific mAChRs with high selectivity.”

89
Q

what are the two binding sites of muscarinic receptors? what binds to each?

A

orthosteric and allosteric

orthosteric: conventional muscarinic receptor ligands

allosteric site: newer compounds can bind to one or both simultaneously (bitopic ligands)

90
Q

what are bitopic ligands referring to?

A

compounds which can bind to both allosteric and orthorsteric binding sites of muscarinic receptors simultaneously.

91
Q

what do allosteric ligands do?

A

promote conformational changes in receptor that manifest as alternation in properties of ligand bound to orthosteric (classic) site.

92
Q

orthosteric vs. allosteric?

A

orthosteric relates to original binding site directly, while allosteric is another site that cause conformational changes and cause indirect effects.

93
Q

types of allosteric modulators:

A

positive allosteric modulator (PAM): enhance orthosteric activity

negative allosteric modulator (NAM): inhibit orthosteric activity

neutral allosteric modulator (NAL): do not change orthosteric activity.

94
Q

compared to muscarinic ligands, what is one reason allosteric modulators may be better for treatment?

A

provide more selective muscarinic ligands than those currently available –> fewer side effects.

Pharmacology (5 decks)

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