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psc3011 - gastrointestinal tract 1 > lecture 17 > Flashcards

lecture 17 Flashcards

1
Q

what are the hormones found in the GI tract?

A
  • secretin
  • gastro inhibitory peptide (GIP)
  • glucagon
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2
Q

where are these hormones located?

A
  • epithelial endocrine cells
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3
Q

what are the neurotransmitters in the GI tract?

A
  • VIP (vasoactive intestinal polypeptide)
  • PHI (peptide histidine isoleucine)
  • PACAP
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4
Q

what is VIP?

A
  • vasoactive inhibitory peptide
  • peptide hormone that’s vasoactive in the intestine
  • 28 amino acids long
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5
Q

what is VIP involved in?

A
  • digestion
  • vasodilation
  • blood flow
  • causes decrease in blood pressure-relaxes smooth muscle
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6
Q

what is PHI structure?

A
  • 27 amino acids long
  • histidine at position 1
  • isoleucine at position 27
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7
Q

which neurotransmitters are coreleased and cotransported?

A
  • VIP and PHI
  • 13 amino acids similarity (similar biological properties)
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8
Q

what amino acid do all have in common?

A
  • phenylalanine at positon 6
  • important in binding to the receptor
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9
Q

what amino acid do all lack?

A
  • cysteine
  • suggests flexible structure
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10
Q

what is required for functioning of the VIP family?

A
  • whole sequence
  • suggests no active site
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11
Q

what is the criteria for chemical neurotransmission?

A
  1. found in neurones, biosynthesis mechanisms present
  2. concentrated in nerve terminals, released by depolarising nerve stimulation
  3. application of exogenous material mimics response caused by nerve stimulation
  4. antagonists have same effect on both exogenous and endogenous effects
  5. mechanisms of breakdown, removal or re-uptake need to be present
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12
Q

what does bolus formation stimulus cause?

A
  • distension of muscle layers
  • activates afferent neurones
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13
Q

where do the afferent neurones extend?

A
  • into myenteric plexus
  • in orad to caudad direction
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14
Q

what do the afferent neurones synapse onto?

A
  • interneurones
  • efferent neurones
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15
Q

what is the function of interneurones in bolus movement?

A
  • passed down myenteric plexus
  • release output into myenteric plexus (VIP)
  • causes ascending relaxation
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16
Q

what is the function of motor neurones in bolus movement?

A
  • extend into the circular muscle
  • release neurotransmitter
  • causes descending contraction
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17
Q

what is the process of bolus movement?

A
  • stimulus = bolus distension
  • activates afferent neurones in myenteric plexus which synapse
  • causes efferent neurones to go into circular muscle and release VIP
  • descending contraction
  • bolus moves forward (waves of activity)
  • neurones fire onto different efferent neurones/interneurones
  • wave of activity moves along circular muscle causing relaxation in waves
  • bolus movement
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18
Q

what happens once the bolus moves?

A
  • stimulates the next segment of neurones
  • wave moving forward
  • relaxation infront, contraction behind
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19
Q

where is VIP found?

A
  • in efferent motor neurones in cell body
  • in nerve terminals which extend into circular muscle layers
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20
Q

what are VIP blood levels?

A
  • low
  • no large fluctuations
  • VIP represents overflow of neurotransmitter
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21
Q

what did Fahrenkrug 1978 experiment set out to look at?

A
  • inhibitory responses in gut motility
  • looks at receptive relaxation stimulated by mechanical stimulation of pharynx and oesophagus when swallow
  • long reflex (involves vagovagal reflex)
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22
Q

what is the vasovagal reflex?

A
  • GI reflects circuit where afferent and efferent fibres of vagus nerve coordinate responses to gut stimuli
  • via dorsal vagal complex in the brain
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23
Q

what treatment doesnt block the response?

A
  • standard cholinergic muscarinic blockers (eg. atropine/adrenergic receptor blockers)
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24
Q

what does the lack of response to this treatment suggest?

A
  • non adrenergic non cholinergic response
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25
Q

what inhibits the inhibitory response?

A
  • hexamethonium
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26
Q

what does this inhibition suggest?

A
  • role of interneurone as blocks cholinergic receptors
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27
Q

what occurs in the Fahrenkrug experiment?

A
  • directly stimulate vagus nerve in neck to mimic effects of vagus nerve
  • or mechanically stimulate the pharynx
28
Q

what occurs with electrical/vagal stimulation?

A
  • increase in VIP in blood leaving stomach
  • increased volume of stomach (relaxation)
  • mimics receptive relaxation
  • long reflex
29
Q

how is the mechanical stimulation achieved?

A
  • balloon placed in pharynx
  • filled with saline
  • as balloon expands, stimulates a swallowing response
  • oesophageal distension
30
Q

what are the results from the mechanical stimulation?

A
  • increased VIP in blood leaving stomach
  • increased relaxation
31
Q

what does this experiment show?

A
  • link between VIP and stomach relaxation
32
Q

what did Grider 1985 test for?

A
  • to study contributions of VIP and ATP to relaxation of smooth muscle
33
Q

why are VIP and ATP the two main candidate neurotransmitters?

A
  • both found in neurones throughout gut
  • both have direct relaxant effects on GI smooth muscle
34
Q

what occurred pre-method in Grider 1985?

A
  • strips taken from stomach of guinea pig
  • treated with atropine to block muscarinic cholinergic responses
  • treated with guanethidine to block adrenergic effects
35
Q

what is the method for Grider?

A
  • either side of stomach strip attached by thread
  • one end attached to tissue bath
  • other attached to tension transducer
  • filled bath with Krebs ringers solution to keep tissue alive
36
Q

what happens when exogenous VIP was added?

A
  • shows dose/conc dependent increases in relaxation
37
Q

what happens when exogenous VIP antibody was added?

A
  • reduced response
  • antibody binds VIP so less VIP binds to its receptor
  • shows VIP has receptor on muscle cells to cause relaxation
38
Q

what happens when exogenous ATP Is added?

A
  • increased relaxation with increasing ATP
39
Q

what happens when exogenous BzATP (ATP antagonist) is added?

A
  • reduces the effects of ATP on muscle relaxation
40
Q

how is the effect of endogenous substrates tested?

A
  • by field stimulation
  • electrodes placed either side of tissue in tissue bath
  • current passed along stimulating nervous system
  • releases neurotransmitters
41
Q

what does increased cycle frequency of stimulation mean?

A
  • tissue relaxes
  • endogenous neurotransmitters are released
42
Q

what occurs when VIP antibody is added?

A
  • blocks part of the response
  • big decrease in relaxation
43
Q

what does this blockage by VIP antiserum suggest?

A
  • when tissue extends endogenously, VIP is released not ATP
44
Q

what happened when BzATP was added?

A
  • no effect
45
Q

what do Grider and Makhlouf test?

A
  • peristaltic type reflexes
  • investigates two parts of peristaltic reflex at once
46
Q

what is the Grider and Makhlouf experiment method?

A
  • take tube of colon tissue
  • place glass rod through the colon
  • attach one end to the tissue bath
  • add tension transducer at orad -> caudad end
  • pulley system added in middle to allow tissue stretch
47
Q

what occurs when orad stretch is stimulated?

A
  • the more stretch , the greater the descending relaxation
48
Q

what can this Grider and Makhlouf response be blocked by?

A
  • tetrodotoxin (inhibits Na+ channels)
49
Q

what occurs when stretch its stimulated at the caudad end?

A
  • no increase in VIP release
50
Q

what does this tell us?

A
  • stretching also causes damage
  • stops neurotransmitter release
51
Q

what did Grider and RIvier test?

A
  • whether stretch and relaxation are linked
52
Q

what were the results from Grider and Riviers experiment?

A
  • VIP antiserum and BzATP cause reduced relaxation
  • for control, greater the stretch = greater the relaxation
53
Q

what does the VIP antiserum response suggest?

A
  • VIP has to be released before the relaxation
  • VIP antibody only works when been released from the tissue
  • blocks the response
54
Q

what does the response suggest about VIP 10-28?

A
  • blocks receptor but doesnt activate
  • more inhibition response
55
Q

how are the effects of PHI tested by Grider and Rivier?

A
  • antibody highly specific for VIP added so mops up the VIP
  • leaves the effects of PHI
56
Q

why is using an antagonist more effective than using an antibody?

A
  • antagonist blocks the effects of anything using the receptor
  • effects both VIP and PHI
57
Q

what is the main receptor for VIP/PHI/PACAP?

A
  • VPAC2 (receptor expressed on smooth muscle)
58
Q

what experiment was carried out by Grider and Rivier involving VIP and PHI?

A
  • added different exogenous compounds and looked at effects of inhibitors
  • measured relaxation
59
Q

what occurs with presence of exogenous VIP/PHI and antibody?

A
  • blocks VIP response
  • little effect of PHI
60
Q

what other substance do neurones contain?

A
  • nitric oxide synthase (NOS)
61
Q

what is NO used for?

A
  • relaxant agent on smooth muscle
62
Q

how is NO produced?

A
  • arginine converted to NO + citrolline by NOS
63
Q

what occurs with NO and tissue relaxation?

A
  • if stimulate relaxation, NO is released
  • oxyhemoglobin added to tissue bath, blocks NANC responses and binds NO
64
Q

how does exogenous NO cause relaxation of GI smooth muscle?

A
  • increases tissue cGMP levels
  • increases intracellular Ca2+
  • K+ channel opens
  • rapid hyperpolarisation
  • relaxation
65
Q

what did Grider test in 1992?

A
  • stimulating muscle strips (1) by field stimulation to measure released neurotransmitters
  • testing isolated cells (2) with different substrates
66
Q

what occurred in experiment 1 including muscle strips?

A
  • field stimulation = increase all
  • +L-NNA = decreased relaxation. decreased VIP release, inhibited NO production
  • +L-arginine = increase in all
67
Q

what occurs in experiment two with isolated muscle cells?

A
  • non had effect on VIP release
  • +exogenous VIP = increase relaxation and NO production
    • L-NNA = decreased relaxation, inhibited NO production
  • +L-arginine = increased both

psc3011 - gastrointestinal tract 1 (5 decks)

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