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Physiology and Pharmacology > The Autonomic Nervous System and Pharmacology > Flashcards

The Autonomic Nervous System and Pharmacology Flashcards

1
Q

why is the ANS important?

A
  • ensures we survive despite lack of consciousness and cortical input
  • self-governing when we sleep
    maintains homeostasis
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2
Q

what are the 4 major components of the nervous system?

A
  1. sensory/afferent PNS:
    - somatic nervous system - receptive to stimuli on skin/muscles
    - visceral nerves - receptive to things entering organs
  2. CNS - brain and spinal cord
  3. Motor/efferent PNS:
    - somatic nervous system - voluntary
    - ANS - involuntary
  4. effectors
    - somatic = skeletal muscle
    - autonomic = smooth muscle, cardiac muscle, glands
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3
Q

what are the 2 major pathways of the ANS?

A
  1. sympathetic (fight or flight)
    - activated during exercise, excitement, emergency, embarrassment
    - can be whole body or organ specific response
  2. parasympathetic (rest and digest)
    - activated during digestion, defecation and diuresis
    - functions in discrete, organ specific manner
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4
Q

what does the sympathetic nervous system stimulate?

A
  • dilation of pupils
  • increase in heart rate and contractility
  • vasodilation of blood vessels to muscles by contraction of smooth muscle
  • vasoconstriction of blood vessels to gut
  • contraction of smooth muscle in bronchioles to widen airways
  • breakdown of glucose in liver
  • ejaculation and orgasm
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5
Q

what does the parasympathetic nervous system stimulate?

A
  • constriction of pupils
  • slowing of heart rate (doesn’t change contractility)
  • vasodilation to GI tract
  • release of enzymes and bile in GI tract
  • bladder wall contraction and sphincter relaxation to allow urination
  • arousal
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6
Q

how do sympathetic and parasympathetic innervations work in relation to one another?

A
  • they innervate the same tissues but have opposing effects
  • antagonistic actions but work synergistically - one increases, the other decreases
  • rapid, precise control of tissue function
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7
Q

which tissues are stimulated by sympathetic innervation only?

A
  • sweat glands, hair follicles, blood vessel smooth muscle and adrenal medulla
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8
Q

What is the general organisation of the ANS? (both sympathetic and parasympathetic)

A
  • preganglionic neuron located in the CNS
  • preganglionic neuron innervates a postganglionic neuron in the PNS (peripheral ganglion)
  • postganglionic neuron innervates a target cell

except adrenal medulla in sympathetic pathway (preganglionic to target cell)

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9
Q

what are preganglionic neurons?

A
  • always cholinergic neurons (ACh is neurotransmitter)
  • ACh activates ionotropic nAChRs on postsynaptic membrane
  • this allows ions to move into the postganglionic neuron and excite it
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10
Q

what is the organisation of the sympathetic pathway?

A
  • short, cholinergic preganglionic neurons originate from T1 to L3
  • long adrenergic postganglionic neurons release noradrenalin to target cells
  • target cells express metabotropic alpha and beta adrenergic receptors
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11
Q

how does the sympathetic nervous system innervate the adrenal medulla?

A
  • chromaffin cells (preganglionic neurons) function similarly to postganglionic neurons but release adrenaline which moves into blood stream
  • this leads to a broad sympathetic response throughout the body
  • adrenaline acts as a neurohormone as it is released neuronally but dispersed hormonally
  • target tissues express alpha and beta adrenergic receptors
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12
Q

what is the organisation of the parasympathetic pathway?

A
  • long, cholinergic preganglionic neurons from brain stem and sacral spinal cord
  • short, cholinergic postganglionic neurons release ACh to target cells
  • target cells express metabotropic mAChRs (muscarinic)
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13
Q

why is the vagus nerve important?

A
  • also called Cranial Nerve X
  • carries around 80& of parasympathetic outflow
  • carries tonnes of visceral afferents
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14
Q

what are the 2 essential components of the ANS?

A
  1. spinal cord
    - cell bodies of preganglionic neurons are located in the lateral horn
    - mediates autonomic reflexes
    - receives sensory afferent and brainstem input
  2. brainstem nuclei
    - mediate autonomic reflexes
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15
Q

how is the hypothalamus used in the ANS?

A
  1. feeding
  2. thermoregulation
  3. circadian rhythms
  4. water balance
  5. sexual drive
  6. reproduction, birth and lactation
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16
Q

what else regulates ANS output?

A

forebrain:

  • minimal conscious cortical control regulates output
  • e.g. anxiety/stress leads to GI disturbance
  • e.g. fear leads to fight or flight response (limbic system)

visceral afferents:

  • sensory input from visceral afferents takes priority over cortical functions
  • e.g. bladder distension
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17
Q

what are the 2 principle neurotransmitters in the ANS?

A
  • acetylcholine (ACh)

- noradrenalin (NA)

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18
Q

what receptors does ACh act upon?

A
  1. nicotinic ACh receptors (nAChRs) - ionotropic
    - found in preganglionic -> postganglionic communication
  2. muscarinic ACh receptors (mAChRs) - metabotropic
    - found on organs via the parasympathetic system (and sweat glands in sympathetic)
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19
Q

what receptors does NA act upon?

A
  • alpha adrenoreceptors
  • beta adrenoreceptors
  • both are metabotropic and are found upon chromaffin cells
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20
Q

what is the principle neurotransmitter of the sympathetic nervous system?

A
  • most organs are innervated by NA

- (except sweat glands and adrenal medulla which use ACh)

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21
Q

what is the principle neurotransmitter of the parasympathetic nervous system?

A
  • ACh to innervate mAChRs on target tissues
22
Q

what discoveries did Dale make about the activity of ACh?

A
  • muscarinic actions resemble effects of parasympathetic innervation
  • atropine blocks muscarinic effects
  • curare blocks effect of nicotine and ACh on nAChRs
23
Q

what effects do large doses of ACh produce, once muscarinic effects have been blocked by atropine?

A
  1. stimulation of all autonomic ganglia
  2. stimulation of voluntary muscle
  3. secretion of adrenaline from adrenal medulla
24
Q

what are the different subtypes of mAChRs?

A

M1, M2, M3, M4, M5

25
Q

what are M1 receptors?

A

M1 (neural): coupled to Gq-protein

  • activate PLC, IP3 and intracellular Ca2+ influx
  • common to all postsynaptic mAChRs, autonomic ganglia, glands and cerebral cortex
26
Q

what are M2 receptors?

A

M2 (cardiac): coupled to Gi- protein

  • inhibit adenylyl cyclase, decrease cAMP, open GIRK channels, inhibit Ca2+ channels due to less PKA activity
  • found in atria of heart
27
Q

what are M3 receptors?

A

smooth muscle: coupled to Gq-protein

  • found on endothelial cells
  • regulates production of nitric oxide which causes vasodilation and drop in blood pressure
  • innervate exocrine glands, smooth muscle, eye, airways, bladder
28
Q

what are M4 receptors?

A
  • coupled to Gi-proteins

- found in CNS

29
Q

what are M5 receptors?

A
  • coupled to Gq-proteins

- located in substantia nigra, salivary glands and CNS

30
Q

how do M2 ACh receptors work on cardiac muscle?

A
  • M2 receptors are negatively coupled to adenylyl cyclase through Gi protein and reduce cAMP formation
  • this inhibits opening of L-type calcium channels, slowing Ca2+ influx
  • M2 receptors open GIRK channels via beta-gamma subunits
  • causes an increase in K+ permeability, causing hyperpolarisation of atria
  • causes heart rate to slow
31
Q

how do M2 receptors mediate effects of pilocarpine agonist?

A
  • pilocarpine opens GIRK channels via beta-gamma subunit binding
  • causes hyperpolarisation of pacemaker and slows AP firing
  • causes slowing of heart
32
Q

what are the actions of M1 and M3 ACh receptors?

A

they are Gq coupled receptors

they:
1. increase bronchoconstriction
2. increase GI motility
3. increase secretion from exocrine glands so increase mucus in lungs

33
Q

what are the affects of agonist muscarine on mAChRs?

A
  • eating over a gram causes nausea
  • decrease in blood pressure is due to decrease in cardiac output (M2) and increased nitric oxide production by endothelial cells (M3)
  • increase in saliva, tear-flow, sweating and abdominal pain (M3)
34
Q

what is cevimeline?

A

an M3 selective agonist which is used to improve salivary and lacrimal secretions in Sjogrens syndrome

35
Q

what is glaucoma? how can glaucoma be treated?

A
  • an eye condition that can cause blindness due to drainage tubes in the eye becoming blocked
  • build up on intraocular pressure can damage the optic nerve
  • pilocarpine (muscarinic agonist) eye drops are used to reduce pressure inside the eye by increasing drainage from eye into bloodstream
36
Q

give an example of a muscarinic antagonist and its effects:

A

atropine:

  • inhibition of secretion of saliva and mucus
  • smooth muscle relaxant of blood vessels and bronchioles
  • pupillary dilation
  • increase in heart rate
  • decrease in GI motility and acid secretion
  • CNS agitation and disorientation
  • increase in body temperature
37
Q

what is Pirenzipine?

A
  • M1 selective antagonist used to treat peptic ulcers

- controls acid secretion in the gut

38
Q

what is darifenacin?

A
  • M3 selective antagonist used to treat overactive bladder

- relaxes smooth muscle of the bladder

39
Q

what are cholinomimetic drugs?

A

they mimic the effects of activating the cholinergic pathway

  • they inhibit AChE to indirectly increase ACh levels to increase activation of cholinergic receptors
  • they can increase activity of both mAChRs and nAChRs
40
Q

which cholinomimetic drugs inhibit AChE?

A

physostigm-ine is an AChE drug used to treat glaucoma
- sarin (nerve gas), organophosphate pesticides are used as poisons to inhibit AChE, leading to build up of ACh and activate cholinergic receptors

41
Q

where are receptors for NA found?

A
  • tissues that respond to postganglionic sympathetic neurons

- smooth muscle, cardiac muscle, glands

42
Q

what are alpha and beta adrenoreceptors involved in?

A

alpha 1 = vasoconstriction of blood vessels
alpha 2 = clot formation

beta 1 = increased contractility of heart
beta 2 = dilation and relaxation of smooth muscle in airways

43
Q

which adrenoreceptor is targeted to treat asthma?

A

beta 2

44
Q

how are receptors classified?

A
  • by their signalling mechanism, pharmacology and which G-protein they are coupled to

alpha 1 = due to NA being found to be more potent than adrenaline, coupled to Gq, increase in Ca2+ and so more contraction

alpha 2 - increased sensitivity to adrenaline over NA, coupled to Gi

beta = more potent for isoprenaline, coupled to Gs, increase in cAMP production

45
Q

how do beta-1 adrenoreceptors cause increase in heart rate?

A
  • coupled to Gs protein
  • increase in cAMP to activate PKA to open L-type calcium channels, causing influx of Ca2+ into cardiac muscle, thus depolarisation and increased contraction
46
Q

what are the clinical uses of adrenaline?

A

adrenaline is an endogenous agonist

  • released by chromaffin cells of adrenal gland
  • affects all adrenoreceptors

found in EpiPens to treat anyphalactic shock - drop in blood pressure

  • causes increase in heart rate and stronger contractions
  • treats cardiac arrest
47
Q

how does salbutamol affect beta-2 adrenoreceptors?

A
  • it is an agonist that causes bronchodilation of airways

- used in inhalers to treat asthma

48
Q

what does ephedrine do?

A
  • nasal decongestant
  • causes constriction of smooth muscle lining the arteries to reduce leakage
  • indirectly acting sympathetic drug (sympathomimetic) which causes NA release
49
Q

what are amphetamines?

A
  • indirect sympathomimetic drug (mimics effects of increased sympathetic signalling via NA)
  • they are taken up by trnasporters in plasma membrane of NA neurons
  • structurally related to NA, dopamine and 5-HT
50
Q

how does amphetamine increase NA action

A
  • inhibits enzymes which hydrolyse NA
  • binds to NA recycling transporters to prevent NA being taken back up into cell, allowing it to accumulate in cleft and innervate target tissues
51
Q

what are prazosin, carvedilol and propranolol? what are their actions?

A

antagonists of adrenoreceptors (they are beta blockers)

  1. prazosin: alpha-1 selective
    - combats vasoconstriction and hypertension
  2. carvedilol: alpha and beta selective
    - decreases workload of heart to combat heart failure
  3. propranolol: beta-1 and beta-2 selective
    - relieves fast breathing and increased heart rate to treat anxiety
52
Q

what are the unwanted effects of beta blockers?

A
  • bronchoconstriction
  • can be fatal for asthma patients
  • cardiac depression and exacerbations
  • brachycardia - reduced cardiac output
  • fatigure
  • cold extremities due to loss of beta-receptor mediated vasodilation

Physiology and Pharmacology (13 decks)

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