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ESA 2 > M&R Session 10: autonomic nervous system > Flashcards

M&R Session 10: autonomic nervous system Flashcards

1
Q

ANS functions?

A

Controls all involuntary functions
Separate from voluntary (somatic) system
Entirely efferent, but regulated by afferent inputs

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2
Q

Sympathetic division?

A

Fight or flight

Increase HR, force of contraction and blood pressure, pupils dilate, adrenaline release, sweating

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3
Q

Parasympathetic division?

A

Regulates basal activities-“rest and digest”

Largely has effects opposing the sympathetic system

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4
Q

Parasympathetic nerve characteristics

A

Originate in lateral horn of medulla and sacral region of spinal cord
Long myelinated pre-ganglionic neurones, short unmyelinated post-ganglionic neurones
Ganglia in tissues innervated by postsynaptic fibres

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5
Q

Sympathetic nerve characteristics

A

Originate in lateral horn of the lumbar and thoracic spinal cord
Short myelinated pre-ganglionic neurones, long unmyelinated post-ganglionic neurones
Ganglia in the paravertebral chain close to the spinal cord

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6
Q

Neurotransmitter and receptors for all pre-ganglionic neurones?

A

All are cholinergic (use ACh)

So cause activation of post-ganglionic nicotinic ACh receptors (ligand-gated ion channels)

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7
Q

Neurotransmitter and receptors for parasympathetic post-ganglionic neurones?

A

Cholinergic: use ACh

Acts on muscarinic ACh receptors in the target tissue (GPCRs. 5 types)

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8
Q

Neurotransmitter and receptors for sympathetic post-ganglionic neurones?

A

Most:
Noradrenergic: use noradrenaline which acts on alpha or beta adrenoceptors (9 types, further subdivided, GPCRs)

Some:
Cholinergic: use ACh to act on mAChR
e.g. sweat glands, hair follicles (piloerection)

Adrenal glands different-release adrenaline into blood rather than target tissue. The sympathetic postganglionic neurones here differentiate to form neurosecretory chromaffin cells

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9
Q

Non-adrenergic, non-cholinergic transmitters?

A

May be co-released with either NA or ACh

Examples:
ATP
nitric oxide
5-hydroxytryptamine (serotonin)
neuropeptides such as VIP
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10
Q

Parasympathetic release of ACh effect on heart + receptors

A

M2 muscarinic ACh receptors activated, causing:

  • bradycardia (act on SA node to decrease beats)
  • reduced conduction velocity (act on AV node to decrease conduction from atria to ventricles)
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11
Q

Parasympathetic release of ACh effect on smooth muscle + receptors

A

M3 muscarinic ACh receptors
Lungs: bronchial and bronchiolar contraction
GI tract: increased intestinal mobility and secretion
GU tract: bladder contraction (detrusor) and relaxation (sphincter). Also penile erection but via NO: ACh causes NO release which causes the erection
Eye: ciliary muscle and iris sphincter contraction

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12
Q

Parasympathetic release of ACh effect on glands and receptor

A

M1 and M3 muscarinic ACh receptors

Increased sweat/salivary/lacrimal secretions

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13
Q

Sympathetic release of NA effect and receptor-heart

A

Positive chronotropy-tachycardia-from SA node
Positive inotropy-increase FoC-from ventricles
B1 receptors (B2)

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14
Q

Sympathetic release of NA effect and receptor-smooth muscle

A

Arteriolar contraction/venous contraction-a1 adrenoceptors
Some arteriolar relaxation in exercising muscle to run fast-so b2 adrenoceptors here to relax
Bronchiolar/intestinal/uterine relaxation: b2 (b3) adrenoceptors
Bladder sphincter contraction-b3 adrenoceptors
Radial muscle contraction-a1 adrenoreceptors

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15
Q

Sympathetic release of NA effect and receptor-kidney

A

Renin release

b1 and b2 adrenoreceptors

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16
Q

Sympathetic release of NA effect and receptor-glandular

A

Increased viscous secretions

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17
Q

Describe the afferent (sensory) inputs to the ANS

A
  • Sensory neurones monitor levels of CO2, O2, nutrients in blood, arterial pressure, and GI tract content
  • blood composition also sensed by the carotid body (chemoreceptors of carotid artery): send info to CNS via glossopharyngeal nerve
  • nucleus tractus solitarius: integrates all visceral afferent info
  • this also receives input from the area postrema (detects blood and CSF toxins)
18
Q

What is dysautonomia?

A

Distinct malfunctions of the ANS

19
Q

Catecholamine disorders?

A

Pheohromocytoma

Baroreflex failure

20
Q

Central autonomic disorders?

A

Mutiple system atrophy:

21
Q

Peripheral autonomic disorders?

A

Guillain-Barre syndrome

Familial dysautonomia

22
Q

Orthostatic intolerance syndromes?

A

Postural orthostatic tachycardia syndrome (POTS)

23
Q

Paroxysmal autonomic syncopes?

A

Neurocardiogenic syncope

24
Q

List the basic steps in neurotransmission, indicating which are the most common sites of drug action (*)

A
  1. Uptake of precursors
  2. Synthesis of transmitter
  3. Vesicular storage of transmitter
  4. Degradation of transmitter *
  5. Depolarisation by propagated action potential
  6. Depolarisation-dependent influx of Ca2+
  7. Exocytotic release of transmitter
  8. Diffusion to post-synaptic membrane
  9. Interaction with post-synaptic receptors*
  10. Inactivation of transmitter*
  11. Re-uptake of transmitter*
  12. Interaction with pre-synaptic receptors*
25
Q

Manipulating cholinergic function?

A

Interfere at nicotinic ganglia-there will not be discrimination between sympathetic and parasympathetic
Interfere at muscarinic receptors: more selective, mainly parasympathetic effects

26
Q

How is ACh synthesised?

A

acetyl CoA + choline –> acetylcholine + coenzyme A

Via choline acetyltransferase

27
Q

How is ACh degraded?

A

acetylcholine –> acetate + choline

Via acetylcholinesterase

28
Q

How can nAChRs be targeted?

A

Differ in structure at autonomic ganglia and the neuromuscular junction
So some drugs select for autonomic ganglia action: e.g. tripemethaphan (blocks ganglia) used in hypertensive emergencies. But undesirable side effects

29
Q

How can mAChRs be targeted?

A

5 subtypes (M1-M5), but only a few subtype-selective agonists/antagonists currently available

Agonists: pilocarpine (glaucoma), bethanechol (stimulate bladder emptying)

Antagonists: ipratropium and tiotropium (COPD), tolterodine, darifenacin and oxybutynin (overactive bladder)

30
Q

How can AChE inhibitors be used therapeutically?

A

Enhance the actions of endogenous ACh by preventing breakdown
E.g. pyridostigmine (myasthenia gravis) and donepezil (Alzheimer’s disease)

31
Q

Side effects of non-selective muscarinic ACh receptor agonists?

A

Heat: decrease HR and output
Smooth muscle: increase bronchoconstriction and peristalsis
Exocrine glands: increase sweating and salivation
“Sludge syndrome”

32
Q

Describe the synthesis of noradrenaline

A
  1. Tyrosine to DOPA by tyrosine hydroxylase DOPA a drug itself for Parkinson’s treatment
  2. DOPA to dopamine by DOPA decarboxylase. Dopamine moved from cytosol into vesicles
  3. Dopamine to noradrenaline by dopamine beta-hydroxylase
33
Q

What happens after Ca2+-dependent exocytotic release of NA?

A
  1. NA diffuses across synaptic cleft to interact with adrenoceptors in post-synaptic membrane to initiate signalling in effector
  2. NA interacts with pre-synaptic adrenoceptors to regulate processes within the nerve terminal

Only limited time for effects as rapidly removed by noradrenaline transporter proteins

34
Q

Termination of noradrenergic transmission?

A

Uptake 1: re-uptake into pre-synaptic terminal by this Na+-dependent, high affinity transporter (most)
Uptake 2: residual NA taken up by a combination of lower-affinity, non-neuronal mechanisms

35
Q

Metabolism of NA?

A

Within the pre-synaptic terminal, NA not taken up into vesicles is metabolised by:

  • monoamine oxidase (MAO)
  • catechol-O-methyltransferase (COMT)
36
Q

How can presynaptic GPCRs e.g. a2 adrenoceptor regulate neurotransmitter release?

A

Inhibit Ca2+-dependent exocytosis:

G protein betagamma subunits inhibit specific types of VOCCs thus reducing Ca2+ influx and neurotransmitter release

37
Q

Indirectly-acting sympathomimetric agents?

A

E.g. tyramine, amphetamine, ephedrine

Taken up into NA synaptic vesicles, NA leaks from vesicle, then leaks into synaptic cleft

38
Q

Uptake 1 inhibitors?

A

E.g. tricylclic antidepressents, selective NA reuptake inhibitors

Exert ajor effects in CNS. Unwanted peripheral side effects can be minimised by choice of drug and dose

39
Q

Salbutamol in asthma effect?

A

It is a beta 2 adrenoceptor-selective agonist
Relieves bronchoconstriction

The selectivity minimises possible CVS side effects (positive inotropic and chronotropic)

40
Q

Hypertension treatment?

A

Alpha 1 adrenoceptor-selective agonists e.g. doxazosin

Beta 1 adrenoceptor-selective antagonists, e.g. atenolol

41
Q

Chronic heart failure treatment?

A

Beta blocker, ACE inhibitor and diuretic

Beta 1 adrenoceptor selective antagonists e.g. bisoprolol, metoprolol

Mixed alpha1/beta1/beta2 adrenoceptor antagonist-carvedilol. Very useful for chronic heart failure

ESA 2 (58 decks)

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