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Biology > Topic 6 > Flashcards

Topic 6 Flashcards

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1
Q

Nervous communication

A
  • fast
  • short lived
  • localised
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2
Q

Central nervous system

A
  • brain

- spinal cord

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3
Q

Paripheral nervous system

A
  • all other neurones

- autonomic, somatic

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4
Q

Somatic nervous system

A

conscious control eg bicep curl, kicking a ball

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5
Q

Autonomic nervous system

A

Unconscious body activity eg heart rate, breathing rate

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6
Q

Parasympathetic nervous system

A
  • slows something down
  • neurotransmitter is acetychline
  • eg decreasing heart rate
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7
Q

Sympathetic nervous system

A
  • speeds things up
  • neurotransmitter called noradrenaline
  • eg increasing heart rate
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8
Q

Receptor pathway

A

Stimulus -> receptor -> sensory neurone -> relay neurone -> motor neurone -> effector -> response

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9
Q

Receptor

A
  • specific - will only detect one type of stimulus
  • cell or protein
  • transform stimulus into an electrical nerve impluse
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10
Q

Sensory neurone

A
  • single long dendron

- single short axon

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11
Q

Relay neurone

A
  • within the CNS
  • many short dendrites
  • many short axons
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12
Q

Motor neurone

A
  • many short dendrites
  • single long axon
  • ends with a neuromuscular junction
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13
Q

Effector

A
  • muscle

- gland

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14
Q

What is involved in the resting potential

A

1) sodium-potassium pump
2) voltage gated sodium ion channel
3) potassium ion channels

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15
Q

Sodium potassium in resting potential

A
  • active transport
  • 3 sodium OUT
  • 2 potassium IN
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16
Q

Voltage gated sodium ion channel in resting potential

A
  • CLOSED

- membrane is not permeable to NA

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17
Q

Potassium ion channels in resting potential

A
  • OPEN
  • some K diffuse out down the electrochemical gradient
  • doesn’t reach equilibrium because of the positive charge outside
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18
Q

Stages of action potentials

A

1) resting potential
2) generator potential
3) threshold
4) depolarisation
5) repolarisation
6) hyper polarisation

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19
Q

Resting potential stage in action potential

A
  • sodium potassium pump
  • active transport
  • Na OUT
  • K IN
  • some K diffuses out via K channel
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20
Q

Generator potential in action potentials

A
  • weak stimulus
  • some Na channels OPEN
  • some Na diffuses IN
  • does NOT reach threshold
  • Na, K pump restores resting potential
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21
Q

Threshold in action potentials

A
  • generator potential reaches threshold
  • many voltage gate na channels open
  • na diffuses into axon
    Positive feedback
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22
Q

Depolarisation in action potential

A
  • Na channels are open

- Na diffuses in

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23
Q

Repolarisation in action potential

A
  • K channels open
  • K diffuse out
  • voltage gated Na close
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24
Q

Hyperpolarisation in action potentials

A
  • when membrane potential is more negative than resting potential
  • K channels slow to close
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25
Q

What is the refectory period in action potentials

A
  • another action potential cannot be started

- makes action potentials: discrete and unidirectional

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26
Q

All or nothing law

A
  • if a generator potential reaches threshold - triggers an action potential
  • all action potentials are same size
  • strong stimulus generates more frequent action potential
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27
Q

Refectory period

A
  • behind the depolarisation phase of an action potential the membrane is in the refectory period
  • action potential cannot go backwards = unidirectional
  • na ions diffuse along the neurone
  • ahead the action potential the neurone is in resting potential
  • Na will trigger threshold
  • Action potential moves along as a wave o depolarisation
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28
Q

Nodes of ranvier

A
  • gaps in the myelin sheath
  • lots of Na ions and K ion channels
  • depolarisation can only happen at the nodes
  • action potentials jump between in a process called saltatory conduction
  • speed up transmission of nerve impulses
  • cytoplasm conducts enough charge to depolarise the next node
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29
Q

Motor neurone structure

A
  • dendrites
  • cell body
  • myelin sheath
  • nodes of ranvier
  • axon terminal
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30
Q

Myelin sheath

A
  • schwan cells make myelin
  • electrical insulator - prevent depolarisation
  • prevents movement of ions in or out of the membrane
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31
Q

Saltatory conduction

A

When an action potential jumps between nodes of ranvier

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32
Q

Temperature of myelination and saltatory conduction

A
  • higher temperature cause faster speeds of action potential (up to 40C)
  • molecules diffuse faster at higher temperatures (more kinetic energy)
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33
Q

Diameter of the axon

A
  • greater the diameter the faster the speed of action potential
  • less resistance
  • more surface area for ion movement
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34
Q

Synapse

A

A junction between neurones

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35
Q

Stages of synapses

A

1) action potential arrives to pre-synaptic knob
2) voltage gated calcium ion channels open - Ca diffuse in
3) vesicles full of neurotransmitters (Ach) fuse with the pre-synaptic membrane
4) Ach diffuses across the synaptic cleft
5) Ach binds with receptors on post synaptic membrane
6) some a channels open
- if threshold is reached
7) voltage gated Na channels open
8) action potential is triggered in the post-synaptic membrane
9) enzyme acetyl cholinesterase breaks down Ach and stops the response
10) products are reabsorbed into the pre-synaptic knob and recycled

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36
Q

Synapses as unidirectional

A
  • only receptors on the post-synaptic membrane
  • neurotransmitters are released from the pre-synaptic knob
  • diffuse from high to low concentration across the synaptic cleft
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37
Q

Temporal summation

A
  • a single action potential doesn’t always trigger an action potential in the post-synaptic membrane
  • a strong stimulus will cause more frequent action potentials
  • release more neurotransmitter
  • adds up to trigger an action potential in post synaptic membrane
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38
Q

Synaptic divergence

A
  • when one neurone joins many neurones

- spreads the action potential to other parts of the body

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39
Q

Synaptic convergence

A
  • when many neurones join a single neurone

- this amplifies the signal

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40
Q

Spatial summation in the role of synapses

A
  • weak stimulus may only create a few action potentials - doesn’t always trigger an action potential in the post synaptic neurone
  • when neurotransmitters from multiple neurones combine to trigger an action potential in a post-synaptic neurone
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41
Q

Neuromuscular junction

A

A synapse between a motor neurone and a muscle fibre

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42
Q

Neuromuscular junctions compared to a cholinergic synapse

A
  • more receptors on the post-synaptic membrane
  • an action potential is ALWAYS generated in the post synaptic membrane
  • Acetycholinesterase is found in pits in the post synaptic membrane (no lingering response)
  • receptors are called nicotinic cholinergic receptors
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43
Q

What occurs at a neuromuscular junction

A
  • wave of depolarisation spreads along the sarcolemma
  • down the transverse tubules
  • to the sarcoplasmic reticulum
  • cause calcium ions to be released
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44
Q

antagonistic pairs

A
  • muscles act in opposite pairs in an incompressible skeleton
  • muscles can only PULL
  • to move a limb in both directions muscles need to work in antagonistic pairs
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45
Q

ligaments

A

attach bones to bones

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46
Q

tendons

A

attach bones to muscles

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47
Q

skeletal/ voluntary muscles facts

A
  • lost of mitochondria
  • long cylindrical cells called muscle fibres
  • muscle fibres are multinucleate (have many nuclei)
  • contain long organelles called myofibrils
  • myofibrils contain myofilaments
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48
Q

sacromere in skeletal muscles

A
  • between the z lines
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49
Q

a band in skeletal muscle

A
  • all of the myosin
  • dark in electromicrograph
  • anchor
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50
Q

h zone in skeletal muscle

A

unoverlapped myosin

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51
Q

i band in skeletal muscle

A
  • actin only
  • doesn’t increase overlap with myosin
  • light in colour
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52
Q

look of actin

A
  • thin

- light

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53
Q

look of myosin

A
  • thick

- dark

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54
Q

z line in skeletal muscle

A

between the i band (actin)

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55
Q

m line in skeletal muscles

A

between the a band (myosin)

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56
Q

relaxed muscle in sliding filament theory

A
  • the actin-myosin binding site is blocked by tropomyosin

- this prevents an actinomyosin bridge being formed

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57
Q

contracting muscle in sliding filament theory

A
  • ca2+ causes tropomyosin to move out of the binding site, allowing actinomyosin bridge to be formed
  • ca2+ also activates ATPase
  • ATP used:
    > change shape of myosin head (continues as long as the binding site is open)
    > detach the myosin head
    > return myosin head to resting/ starting position
    > re-absorb ca2+ into sarcoplasmic reticulum by active transport
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58
Q

sacromere contracted bands

A
  • sacromere - shorter
  • i band - shorter
  • h zone- shorter
  • a band - same
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59
Q

muscle contraction - phosphocreatine

A
  • fastest
  • PCr + ADP -> ATP + Cr
  • phosphate group is added to ADP+ATP
  • cells store PCr
  • short + simple reaction + fastest way to make ATP
  • PCr stores used up quickly
  • used for high intensity, short duration
  • anaerobic
  • alactic (doesn’t make lactic acid)
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60
Q

muscle contraction - anaerobic respiration

A

glycolysis

  • 2 ATP made
  • pyruvate to lactate (causes muscle fatigue)
  • short duration, high intensity (eg 200m)
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61
Q

muscle contraction - aerobic respiration

A
  • slowest
  • lots of ATP mostly by oxidative phosphorylation
  • slow = many reactions -> no harmful waste products
  • eg 10km run
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62
Q

slow twitch muscle fibres

A
  • contract slowly
  • relax slowly
  • force of contraction
  • resistant to fatigue
  • respire aerobically
  • needs lots of: mitochondria, blood vessels, myoglobin
  • little anaerobic respiration
  • eg low intensity, long distance
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63
Q

fast twitch muscle fibres

A
  • contract quickly
  • relax quickly
  • high force of contraction
  • fatigue quickly
  • respire anaerobically
  • has few: mitochondria, blood vessels, myoglobin
  • little aerobic respiration
  • eg high intensity, short duration
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64
Q

Negative feedback

A

Receptors detects a change away from the normal/ optimum and effectors activate mechanisms to return to body to the normal/ optimum

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65
Q

When is negative feedback used

A
  • control and regulation

- example: blood - temp/ph/ glucose

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66
Q

Control of negative feedback

A
  • separate negative feedback systems gives you more control
67
Q

Positive feedback

A

A response that results in the effectors further amplifying the change away from the normal (more produces more)

68
Q

What is positive feedback used for

A
  • rapid changes and responses
  • eg Na+ channels threshold -> depolarisation
  • eg blood clotting
69
Q

Blood glucose control - increase

A

Negative feedback

  • receptors in pancreas detect an increase in blood glucose eg carb rich meal
  • Beta cells in the islets of Langerhans (pancreas) secretes insulin
  • insulin binds to receptors in liver + muscle (increasing permeability to glucose)
  • (then a decrease occurs)
70
Q

What are the responses that come from the liver and muscle tissue after glucose increase

A
  • more glucose is absorbed by facilitated diffusion
  • glycogenesis (glucose to glucogen)
  • increase the rate of respiration
71
Q

What are the responses on the liver after a glucose decrease

A
  • decrease the rate of respiration
  • glycogenolysis (glycogen to glucose)
  • gluconeogenesis (non carbs to glucose)
72
Q

Blood glucose control - decrease

A

Negative feedback

  • receptors in the pancreas detect blood glucose is low eg after exercise
  • Alpha cells in the islets of Langerhans secrete glucagon
  • glucAgon binds to receptors on liver cells
  • (then increase)
73
Q

Glycogenolysis

A
  • the splitting of glycogen
  • glycogen -> glucose
  • promoted by glucagon and adrenaline
74
Q

Glyocgenesis

A
  • Making glycogen
  • promoted by insulin
  • Glucose -> glycogen
75
Q

Glyconeogenesis

A
  • making new glucose
  • promoted by glucagon
  • Non carbohydrates (lipids, amino acids) -> glucose
76
Q

What is glucagon secreted by

A

Alpha cells in the islets of Langerhan (pancreas)

77
Q

What is adrenaline secreted by

A

The adrenal glands

78
Q

What is insulin secreted by

A

Beta cells in the islets of Langerhans (pancreas)

79
Q

What blood glucose concentration is glucagon released at

A

Low concentration

80
Q

What blood glucose concentration is adrenaline released at

A

Low concentration

81
Q

What blood glucose concentration is insulin released at

A

High concentration

82
Q

What receptors does glucagon attach to

A

Liver

83
Q

What receptors does adrenaline attach to

A

Liver

84
Q

What receptors does insulin attach to

A

Liver and muscle

85
Q

Effect of glucagon on blood glucose concentration

A

Increase

86
Q

Effect of adrenaline on blood glucose concentration

A

Increase

87
Q

Effect of insulin on blood glucose concentration

A

Decrease

88
Q

Mechanisms of glycagon

A

1) increase the rate of respiration
2) glycogenolysis (glycogen to glucose)
3) gluconeogenesis (noncarbs to glucose)

89
Q

Mechanisms of insulin

A

1) increase the rate of respiration
2) glycogenesis (glucose->glycogen)
3) increase liver and muscle cells permeability to glucose

90
Q

Mechanism in adrenaline

A
  • Actives: glycogenolysis, secretion of glucagon

- inhibits: glucogenesis, insulin

91
Q

How is the liver and muscle increase there permeability to glucose (insulin)

A
  • glucose carrier proteins are stored in vesicles inside liver and muscle cells
  • insulin binds with receptor on the cell membrane of the target cells, causing the vesicles to fuse with cell membrane
  • carrier proteins join the membrane and glucose is absorbed by facilitated diffusion
92
Q

Diabetes mellitus

A

an illness when blood glucose levels are not controlled

93
Q

Hyperglycaemia

A

Dangerously high blood glucose concentration

94
Q

Hypoglycaemia

A

Dangerously low blood glucose concentration

95
Q

Causes of type 1 diabetes

A

Immune system kills b cells in the islet of Langerhans - can’t make insulin

96
Q

Age of type 1 diabetes

A

Children and young adults

97
Q

Causes of type 2 diabetes

A
  • obesity
  • lack of exercise
  • poor diet
  • b cells don’t make enough insulin
  • liver and muscle cells stop responding to insulin
98
Q

Age for type 2 diabetes

A

Adults/ elderly

99
Q

Type 1 affect on blood glucose

A
  • rise after eating carbohydrates - lead to hyperglycaemia

- stays high - kidneys can’t receive all glucose from urine

100
Q

Type 2 affect on blood glucose

A
  • rise after eating carbohydrate - hyperglycaemia
101
Q

Treatments to type 1

A
  • inject insulin/ pump
  • too much insulin can result in hypoglycaemia
  • avoid simple carbohydrates (sugars)
  • eat at regular intervals
  • regular exercise to use up glucose (less insulin needed)
102
Q

Treatments to type 2

A
  • eat healthily
  • lose weight
  • regular exercise
  • drugs to: reduce the amount of glucose released, increase sensitivity to insulin, make the body produce more insulin
  • insulin injections
103
Q

Second messengers

A

1) hormone eg adrenaline/ glucagon are complementary to the receptor protein on cell membrane of a target cell eg liver cell
2) enzyme (adenyl cyclate) is activated
3) converts ATP -> cAMP (cyclic AMP)
4) cAMP activates an enzyme called protein kinase A by changing its tertiary structure
5) cAMP is a second messenger

104
Q

parts of the nephron

A
  • Glomerulus
  • Afferent arteriole
  • efferent arteriole
  • boumuns capusle
  • proximal conveluted tubule (PCT)
  • Loop of Henle
  • Distal convoluted tublue (DCT)
  • collecting duct
105
Q

proximal convoluted tubule

A
  • most of the reabsorption
  • lost of mitochondria
  • microvilli (large SA)
106
Q

Loop of Henle

A
  • osmoregulation
107
Q

distal convoluted tubule

A
  • reabsorption

- osmoregulation

108
Q

collecting duct

A
  • osmoregulation
109
Q

what is in the medula

A
  • loop of Henle

- collecting duct

110
Q

what is in the cortex

A
  • DCT
  • PCT
  • Glomerulus
  • Bomuns capsule
  • afferent arteriole
  • efferent arteriole
111
Q

ultrification

A
  • high hydrostatic pressure (afferent arteriole is wider than the efferent arteriole)
  • small molecules are forced out into the Bowmans capsule to form the filtrate (glucose, h2o,amino acids, ions, urea)
  • large molecules don’t fit through the gaps: in capillary walls, basement membrane, in podocytes eg red blood cells, protiens
112
Q

Selective reabsorption

A

Useful products are reabsorbed from the glomerulus filtrate mostly by the proximal convoluted tubule and loop of Henle, distal convoluted tubule and collecting duct

113
Q

Stages of selective reabsorption

A
  • ultrafication makes glomerulus filtrate
  • capillaries wrap around the nephron and useful substances are reabsorbed into the blood
  • proximal convoluted tubule absorbs most of the molecules - microvilli increase the surface area for absorption
  • urine is filtrate with useful molecules removed (water, ions, urea, excess vitamins)
114
Q

what are the names of the upper and lower parts of the loop of henle

A
  • upper = cortex

- lower = medula

115
Q

what happens at the ascending limb in the loop of henle

A
  • Na+ cl- pumped OUT
  • Active transport (ATP)
  • decrease the water potential of the medulla
  • impermeable to water (can’t leave via osmosis)
116
Q

what happens at the descending limb of the loop of henle

A
  • permeable to water
  • water moves OUT by osmosis
  • absorbed into capillaries
  • increase concentration of urine
117
Q

what happens at the collecting duct in the loop of henle

A
  • ADH changes its permeability to water
  • more ADH = less piss
  • when ADH is added to a receptor there is more osmosis as it is more permeable to water
118
Q

length of the loop of henle

A
  • the longer the loop of Henle the more concentrated the medulla
  • this means that more water is reabsorbed
  • so there is more concentrated urine (loosing more water)
  • eg desert animals eg camel
  • (long loop = lower water potential of urine)
119
Q

osmoregulation and ADH stages

A

1) dehydrated - blood has a lower water potential
2) detected by osmoreceptors in the hypothalamus
3) posterior pituitary secretes antidiuretic hormone
4) ADH carries in the bloodstream
5) ADH binds to specific receptor proteins on collecting ducts and (DCT)
6) increases the permeability to water
7) water moves OUT of the collecting duct (and DCT) by osmosis (medulla has a very low water potential)

120
Q

osmoregulation summary stages

A

more ADH = collecting duct wall more permeable to water = more water moves OUT of collecting duct by osmosis = less piss

121
Q

Homeostasis

A

Physiological control systems that maintain a constant internal environment

122
Q

Homeostasis - temperature

A
  • metabolism is controlled by enzymes
  • enzymes have an optimum temperature and pH
  • too hot, enzymes denatured
  • too cold, rate of reaction slows down
123
Q

Homeostasis - pH

A
  • metabolism is controlled by enzymes
  • enzymes have an optimum temperature and pH
  • too acid/ alkaline, rate of reaction decreases
124
Q

Homeostasis - glucose

A
  • a minimum amount of glucose is needed as respiratory substrates
  • too much - decrease in water potential of blood
  • water will move out of cells by osmosis
  • cells will shrivel up
125
Q

What is the purpose of growth factors

A

Plants respond to changes in their environment to increase their chance of survival eg towards light to increase rate of photosynthesis

126
Q

Tropism

A

The response of a plant to a directional stimulus

127
Q

Growth factors

A
  • plants respond to stimuli by using growth factors (no circulatory system to nervous system)
  • examples - Auxins (IAA) : shoots = cell elongation (not cell division), gibberellins = flowering and germination
  • made in the growing regions = root tips and shoot tips
128
Q

Movement of growth factors

A
  • move short distances by diffusion and active transport

- move long distances in the phloem

129
Q

Phototropism

A
  • IAA moves to the shaded side of root/ shoot
  • shoots: IAA causes cell elongation - shoots grow towards the light (positive)
  • roots: IAA inhibits cell growth - roots grow away from light (negative)
130
Q

Gravitropism

A
  • IAA always moves to the underside
  • shoots: IAA causes cell elongation - grow away from gravity (negative)
  • roots: IAA inhibits cell growth grow towards gravity (positive)
131
Q

What are taxis and kinesis

A

Are simple responses that keep mobile organisms in favourable environments

132
Q

Taxes

A

Mobile organisms moves towards or away from a directional stimulus eg negative thermotaxes

133
Q

Kinesis

A

Mobile organisms change their movement in response to a non-directional stimulus eg humidity

134
Q

Advantages of taxes

A
  • avoid predators

- reduce water loss

135
Q

Advantages of kinesis

A
  • unfavourable conditions: move more/ faster and turn more = move to a new area
  • favourable conditions: move less/ slower and turns less = remain in the favourable area
136
Q

Choice chamber

A
  • put 100 woodlice in centre of choice chamber
  • observe for 10 mins
  • record the number of turns
  • record the rate of movement
  • record the final position
137
Q

Reflex

A

A rapid response to a stimulus without conscious control

138
Q

Reflex pathway

A

Stimulus -> receptor -> sensory neurone -> relay neurone in CNS -> motor neurone -> response

139
Q

Advantages of reflexes

A
  • help or avoid damage
  • very fast (don’t have to think about it)
  • does not need to be learned (protects infants)
  • eg blinking, knee jerk reflex
140
Q

What does the pacinian corpuscle do

A
  • receptor that detects pressure, touch and vibrations in the skin
141
Q

Pacinian corpuscle diagram

A
142
Q

What occurs at a stimulated pacinian corpuscle

A
  • pressure causes the lamellae to stretch and deform
  • stretch mediated sodium ion channels OPEN
  • Na+ diffuses INTO NEURONE
  • the greater the stimulus the more Na+ channels open
  • depolarisation of the neurone is called generator potential
  • if threshold is reached then an action potential is initiated
143
Q

Parts of the eye

A
  • iris
  • pupil
  • lens
  • retina: fovea, optic nerve
144
Q

Fovea

A
  • lost of photoreceptors

- mostly cones

145
Q

Optic nerve

A
  • blind spot - no photoreceptors
146
Q

What happens at the retina

A
  • light is focused onto the retina by the lens
  • light is absorbed by pigments in the photoreceptors
  • causes some of the sodium ion channels to open (generator potential)
  • if threshold is reached -> action potential -> bipolar neurone -> optic nerve -> CNS
147
Q

Rods

A
  • monochromatic - one pigment (black and white)
  • more sensitive to low light
  • lower visual acuity
  • mostly in peripheral part of the retina
  • get enough stimulus to trigger action potential but only get one action potential
  • many rods join a single bipolar neurone
148
Q

Cones

A
  • trichromatic (red, green, blue optical pigment) = colour vision
  • less sensitive to low light
  • higher visual acuity - each cone has its own bipolar neurone
  • need a stronger stimulus to reach threshold and action potential
  • seperated so can see the resolution/ detail between two points more
149
Q

Atrioventricular valves

A
  • one way valves

- open when blood pressure is higher in the atrium than ventricles

150
Q

Semilunar valves

A
  • one way valves

- open when pressure is greater in ventricles than blood vessels

151
Q

SAN

A
  • initiates heart beat
  • electrical impulse
  • SAN -> AVN
152
Q

AVN

A
  • delay electrical impulse
  • allow atria to contract (empty)
  • before ventricles contract
  • AVN -> Bundle of His -> Purkyne Fibres
153
Q

Purkyne fibres

A
  • electrical impulses causes the ventricles to contract from base upwards
154
Q

Parts of the heart

A
  • Oxygenated blood to body
  • return as deoxygenated through vena cava
  • into right atrium
  • through atrioventricular valves to the right ventricle
  • through semi lunar valves out the pulmonary artery to the lungs
  • return oxygenated through the pulmonary vein
  • into the left atrium
  • through the atrioventricular valves to the left ventricle
  • through the semi lunar valves of the aorta
155
Q

Non-conducting tissue

A

stops the electrical impulse from SAN reaching ventricles

156
Q

Control of heart rate

A
  • SAN initiates the heart beat
  • send an electrical impulse across the atria
  • atria contract
  • non-conductive tissue prevents the electrical impulses reaching the ventricles
  • AVN delays electrical impulse - allows atria to contract and empty before the ventricles contract
  • AVN sends the electrical impulse down the Bundle of His and along the purkyne fibres
  • ventricles contract from the base upwards
157
Q

Left ventricle in the control of heart rate

A
  • highest blood pressure
  • most cardiac muscle
  • contracts with greatest force
  • pumps blood to whole body
158
Q

Atrial systole

A
  • atria = contracts (high bp)
  • ventricles = relaxed (low bp)
  • atrioventricular valve = open
  • semilunar valves = closed
159
Q

Ventricular systole

A
  • atria = relaxed (low bp)
  • ventricles = contracted (high bp)
  • atrioventricular valves = closed
  • semilunar valves = open
160
Q

Diastoyle

A
  • atria = relaxed (low bp)
  • ventricles = relaxed (low)
  • atrioventricular valves = open
    Semilunar valves = closed
161
Q

detection of low blood O2, low pH levels and high CO2

A
  • chemoreceptors detect change in blood
  • impulses sent to medulla, which sends impulses on sympathetic neurones (secrete noradrenaline)
  • effector - cardiac muscle
  • heart rate increases to return levels to normal
162
Q

detection of high blood pressure

A
  • detected by baroreceptors
  • impulses sent to medulla, which send impulses along the parasympathetic neurone (secrete acetylcholine)
  • effector - cardiac muscle
  • heart rate slows down to reduce blood pressure
163
Q

detection of high blood O2, high pH levels and low CO2)

A
  • detected by chemoreceptors
  • impulses sent along the medulla, which sends impulses along parasympathetic neurone (secrete acetylcholine
  • effector - cardiac muscle
  • heart rate decrease to return levels to normal
164
Q

detection of low blood pressure

A
  • detected by baroreceptors
  • impulses sent to medulla, which send impulses long the sympathetic neurone (secrete noradrenaline)
  • effector - cardiac muscle
  • heart rate speeds up to increase blood pressure

Biology (18 decks)

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