Organisms respond to changes in their internal and external environments Flashcards
1
Q
What does Phototropic mean?
A
Stem grows towards the light
2
Q
What does gravitropic mean?
A
Roots are sensitive to gravity and grow in the direction of its pull
3
Q
What is hydrotropic?
A
When almost the plant roots grow towards the water
4
Q
How does IAA control tropisms?
A
1- Cells in root tip produce IAA, which is transported down the shoot, and is initially transported to all sides as it begins to move down
2-Light causes the movement of IAA from the light side to the shaded side of the shoot
3- concentration of IAA builds up on the shaded side than the light side
4- as IAA causes elongation the shaded side begings to elongate more
5- the shaded side begins to bend towards the light
5
Q
What does auxin do?
A
auxin is diffused down the shoot stimulating growth
6
Q
Explain gravitropism
A
-in the roots, a higher concentration of IAA results in a lower rate of cell elongation (inhabition)
-IAA is actively transported to the lower side of the cell therefore there is a higher concentration of IAA which inhibits cell elongation
-so the lower side grows at a slower rate than the upper so the roots bend downwards
7
Q
What is a stimulus?
A
A change in an organisms internal or external enviroment
8
Q
Why is it important for an organism to react to a stimulus?
A
Organisms increase their chance of survival by reponding to a stimulus
9
Q
What is a tropism?
A
Growth of a plant in responce to a directional stimulus
Positive= towards stimulus
Negative= away from stimulus
10
Q
Summarise the role of growth factors in flowering plants?
A
Auxin mves via diffusion from growing regions like the shoot, where they are produced, to other tissue where they regulate growth in responce to directional stimuli (tropism)
11
Q
Describe the simple responce that can maintain a mobile organism in a favourable enviroment?
A
Taxes- directional responce- movement towards or away from diectional stimulus
Kinesis-non directional- speed of movement or directional change responds to non directional stimuli depending on intensity of simulus
12
Q
Explain the protective effect of a simple reflex
A
-Rapid as there is only 3 neurones and a few synapses
-Is automatic as it doesnt involve the brain
-Protects from harmsful stimui- preventing damage to body tissue
13
Q
What is the sensory neurone?
A
A nerve cell that carries impulses from a receptor to the central nervous system
14
Q
What is a motor neurone?
A
A nereve cell that carries impulses from the central nervous system to an effector
15
Q
Explain gravitropism in flowering plants
A
- Cells in tip of shoot / root produce IAA
- IAA diffuses down shoot / root (evenly initially)
- IAA moves to lower side of shoot / root (so concentration increases)
- In shoots this stimulates cell elongation whereas in roots this inhibits cell elongation
- So shoots bend away from gravity whereas roots bend towards gravity
16
Q
Explain phototropism in flowering plants
A
- Cells in tip of shoot / root produce IAA
- IAA diffuses down shoot / root (evenly initially)
- IAA moves to shaded side of shoot / root (so conc. ↑)
- In shoots this stimulates cell elongation whereas in
roots this inhibits cell elongation - So shoots bend towards light
whereas roots bend away from light
17
Q
Describe the basic structure of a Pacinian corpuscle
A
-lamellae, layers of connective tissue
-sensory neurone ending
-sensory nurone axon
-myelin sheath (schwann cells)
-stretch mediated sodium ion channels
18
Q
Describe how a generator potential is established in a Pacinian corpuscle
A
- Mechanical stimulus eg. pressure deforms
lamellae and stretch- mediated sodium ion
(Na+) channels - So Na+ channels in membrane open and Na+ diffuse into sensory neurone
○ Greater pressure causes more Na+ channels to open and more Na + to enter - This causes depolarisation, leading to a generator potential
○ If generator potential reaches threshold it triggers an action potential
19
Q
Explain what the Pacinian corpuscle illustrates
A
● Receptors respond only to specific stimuli
○ Pacinian corpuscle only responds to mechanical pressure
● Stimulation of a receptor leads to the establishment of a generator potential
○ When threshold is reached, action potential sent (all-or-nothing principle)
20
Q
describe the sensitivity to light in Rod cells
A
Rods are more sensitive
● Several rods connected to a single neurone
● Spatial summation to reach / overcome threshold (as enough
neurotransmitter released) to generate an action potential
21
Q
Describe the sensitivity to light in Cone cells
A
Cones are less sensitive to light
● Each cone connected to a
single neurone
● No spatial summation
22
Q
Describe the visual acuity for rod cells
A
Rods give lower visual acuity
● Several rods connected to a single neurone
● So several rods send a single set of impulses
to brain (so can’t distinguish between
separate sources of light)
23
Q
Describe the visual acuity for Cone cells
A
Cones give higher visual acuity
● Each cone connected to a single neurone
● Cones send separate (sets of) impulses to brain
(so can distinguish between 2 separate sources
of light)
24
Q
Explain the sensitivity to colour in rod cells
A
Rods allow
monochromatic vision
● 1 type of rod / 1
pigment
25
Explain the sensitivity to colour in Cone cells
Cones allow colour vision
● 3 types of cones - red-, green- and blue-sensitive
● With different optical pigments → absorb different wavelengths
● Stimulating different combinations of cones gives range of colour perception
26
Describe the myogenic stimulation of the heart and transmission of a
subsequent wave of electrical activity
1 Sinoatrial node (SAN) acts as pacemaker → sends regular waves of electrical activity across atria
○ Causing atria to contract simultaneously
2 Non-conducting tissue between atria / ventricles prevents impulse passing directly to ventricles
○ Preventing immediate contraction of ventricles
3 Waves of electrical activity reach atrioventricular node (AVN) which delays impulse
○ Allowing atria to fully contract and empty before ventricles contract
4 AVN sends wave of electrical activity down bundle of His, conducting wave between ventricles to
apex where it branches into Purkyne tissue
○ Causing ventricles to contract simultaneously from the base up
27
Where are chemoreceptors and pressure receptors located?
Chemoreceptors and pressure receptors are located in the aorta and carotid arteries
28
Describe the roles of chemoreceptors, pressure receptors, the autonomic
nervous system and effectors in controlling heart rate
1. Baroreceptors detect [fall / rise] in blood
pressure and / or chemoreceptors detect
blood [rise / fall] in blood CO2 conc. or [fall
/ rise] in blood pH
2. Send impulses to medulla / cardiac
control centre
3. Which send more frequent impulses to
SAN along [sympathetic /
parasympathetic] neurones
4. So [more / less] frequent impulses sent
from SAN and to / from AVN
5. So cardiac muscle contracts [more / less]
frequently
6. So heart rate [increases / decreases]
29
Describe the structure of a myelinated motor neurone
- dendrite
-cell body
-axon
-myelin sheath made of schwann cells
-nodes of ranvier
-terminal axon
30
Describe resting potential
Inside of axon has a negative charge relative to outside (as more positive ions outside compared to inside).
31
Explain how a resting potential is established across the axon membrane in
a neurone
Na+/K+ pump actively transports:
○ (3) Na+ out of axon AND (2) K+ into axon
● Creating an electrochemical gradient:
○ Higher K+ conc. inside AND higher Na+ conc. outside
● Differential membrane permeability:
○ More permeable to K+ → move out by facilitated diffusion
○ Less permeable to Na+ (closed channels)
32
Explain how changes in membrane permeability lead to depolarisation and
the generation of an action potential
1. Stimulus ● Na+ channels open; membrane permeability to Na+ increases
● Na+ diffuse into axon down electrochemical gradient (causing depolarisation)
2. Depolarisation ● If threshold potential reached, an action potential is generated
● As more voltage-gated Na+ channels open (positive feedback effect)
● So more Na+ diffuse in rapidly
3. Repolarisation ● Voltage-gated Na+ channels close
● Voltage-gated K+ channels open; K+ diffuse out of axon
4. Hyperpolarisation ● K+ channels slow to close so there’s a slight overshoot – too many K+ diffuse out
5. Resting potential ● Restored by Na+/K+ pump
33
Describe the all-or-nothing principle
● For an action potential to be produced, depolarisation must exceed threshold potential
● Action potentials produced are always same magnitude / size / peak at same potential
○ Bigger stimuli instead increase frequency of action potentials
34
Explain how the passage of an action potential along non-myelinated and
myelinated axons results in nerve impulses
Non-myelinated- ● Action potential passes as a wave of
depolarisation
● Influx of Na+ in one region increases permeability of adjoining region to Na+ by causing voltage-gated Na+ channels to open so adjoining region depolarises
Myelinated-● Myelination provides electrical insulation
● Depolarisation of axon at nodes of Ranvier only
● Resulting in saltatory conduction (local currents circuits)
● So there is no need for depolarisation along whole length of axon
35
Suggest how damage to the myelin sheath can lead to slow responses and /
or jerky movement
● Less / no saltatory conduction; depolarisation occurs along whole length of axon
○ So nerve impulses take longer to reach neuromuscular junction; delay in muscle contraction
● Ions / depolarisation may pass / leak to other neur
36
Describe the nature of the refractory period
● Time taken to restore axon to resting potential when no further action potential can be generated
● As Na
+ channels are closed / inactive / will not open
37
Explain the importance of the refractory period
● Ensures discrete impulses are produced (action potentials don’t overlap)
● Limits frequency of impulse transmission at a certain intensity (prevents over reaction to stimulus)
○ Higher intensity stimulus causes higher frequency of action potentials
○ But only up to certain intensity
● Also ensures action potentials travel in one direction – can’t be propagated in a refractory region
38
Describe the factors that affect speed of conductance
-Myelination
● Depolarisation at Nodes of Ranvier only → saltatory conduction
● Impulse doesn’t travel / depolarise whole length of axon
-Axon diameter
● Bigger diameter means less resistance to flow of ions in cytoplasm
-Temperature
● Increases rate of diffusion of Na+ and K+ as more kinetic energy
● But proteins / enzymes could denature at a certain temperature
39
Describe the structure of a synapse
-axon
-voltage gated calcium ion channel
-synaptic cleft
-receptor and sodium ion channel
-axon terminal
-vesicle containing neurotransmitter
40
What are cholinergic synapses?
Synapses that use the neurotransmitter acetylcholine (ACh).
41
Describe transmission across a cholinergic synapse.
At pre-synaptic neurone:
1. Depolarisation of pre-synaptic membrane causes opening of voltage-gated Ca2+ channels
○ Ca2+ diffuse into pre-synaptic neurone / knob
2. Causing vesicles containing ACh to move and fuse with pre-synaptic membrane
○ Releasing ACh into the synaptic cleft (by exocytosis)
At post synaptic neurone;
3. ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane
4. Causing Na+ channels to open
○ Na+ diffuse into post-synaptic knob causing depolarisation
○ If threshold is met, an action potential is initiated
42
Explain what happens to acetylcholine after synaptic transmission
● It is hydrolysed by acetylcholinesterase
● Products are reabsorbed by the presynaptic neurone
● To stop overstimulation - if not removed it would keep binding to receptors, causing depolarisation
43
Explain how synapses result in unidirectional nerve impulses
● Neurotransmitter only made in / released from pre-synaptic neurone
● Receptors only on post-synaptic membrane
44
Explain summation by synapses
● Addition of a number of impulses converging on a single post-synaptic neurone
● Causing rapid buildup of neurotransmitter (NT)
● So threshold more likely to be reached to generate an action potential
45
Describe spatial summation
● Many pre-synaptic neurones share one synaptic cleft / post-synaptic neurone
● Collectively release sufficient NT to reach threshold to trigger an
action potential
46
Describe temporal summation
● One pre-synaptic neurone releases neurotransmitter many times over a short time
● Sufficient NT to reach threshold to trigger an action potential
47
Describe inhibition by inhibitory synapses
● Inhibitory neurotransmitters hyperpolarise postsynaptic membrane as:
○ Cl- channels open → Cl- diffuse in
○ K+ channels open → K+ diffuse out
● More Na+ required for depolarisation
● Reduces likelihood of threshold being met / action potential formation
at post-synaptic membranes
48
Describe the structure of a neuromuscular junction
● Receptors are on muscle fibre instead of postsynaptic membrane and there are more
● Muscle fibre forms clefts to store enzyme eg. acetylcholinesterase to break down neurotransmitter
49
Compare transmission across cholinergic synapses and neuromuscular
junctions
Cholinergic synapse;
-Neurone to neurone (or effectors, glands)
-Neurotransmitters can be excitatory or inhibitory
-Action potential may be initiated in postsynaptic neurone
Neuromuscular junction;
-motor neurone to muscle
- always exictatory
- Action potential propagates along sarcolemmadown T tubules
50
Use examples to explain the effect of drugs on a synapse
● Some drugs stimulate the nervous system, leading to more action potentials, eg.:
○ Similar shape to neurotransmitter
○ Stimulate release of more neurotransmitter
○ Inhibit enzyme that breaks down neurotransmitter → Na+ continues to enter
● Some drugs inhibit the nervous system, leading to fewer action potentials, eg.:
○ Inhibit release of neurotransmitter eg. prevent opening of calcium ion channels
○ Block receptors by mimicking shape of neurotransmitter
51
Describe how muscles work
● Work in antagonistic pairs → pull in opposite directions eg. biceps / triceps
○ One muscle contracts (agonist), pulling on bone / producing force
○ One muscle relaxes (antagonist)
● Skeleton is incompressible so muscle can transmit force to bone
52
Describe the gross and microscopic structure of skeletal muscle
● Made of many bundles of muscle fibres (cells) packaged together
● Attached to bones by tendons
● Muscle fibres contain:
○ Sarcolemma (cell membrane) which folds inwards (invagination) to form transverse (T) tubules
○ Sarcoplasm (cytoplasm)
○ Multiple nuclei
○ Many myofibrils
○ Sarcoplasmic reticulum (endoplasmic reticulum)
○ Many mitochondria
53
Describe the ultrastructure of a myofibril
● Made of two types of long protein filaments, arranged in parallel
○ Myosin - thick filament
○ Actin - thin filament
● Arranged in functional units called sarcomeres
○ Ends – Z-line / disc
○ Middle – M-line
○ H zone – contains only myosin
54
Explain the banding pattern to be seen in myofibrils
● I-bands - light bands containing only thin actin filaments
● A-bands - dark bands containing thick myosin filaments (and some actin filaments)
○ H zone contains only myosin
○ Darkest region contains overlapping actin and myosin
55
Give an overview of muscle contraction
● Myosin heads slide actin along myosin causing the sarcomere to contract
● Simultaneous contraction of many sarcomeres causes myofibrils and muscle fibres to contract
● When sarcomeres contract (shorten)...
○ H zones get shorter
○ I band get shorter
○ A band stays the same
○ Z lines get closer
56
Describe the role of phosphocreatine in muscle contraction
● A source of inorganic phosphate (Pi) → rapidly phosphorylates ADP to regenerate ATP
○ ADP + phosphocreatine → ATP + creatine
● Runs out after a few seconds → used in short bursts of vigorous exercise
● Anaerobic and alactic
57
what are the general properties of a slow twitch muscle
● Specialised for slow, sustained contractions (eg. posture, long distance running)
● Obtain ATP mostly from aerobicrespiration → release energy slowly
● Fatigues slowly
58
Where are slow twitch muscles located?
● High proportion in muscles used for posture eg. back, calves
● Legs of long distance runners
59
Describe the structure of a slow twitch muscle
● High conc. of myoglobin → stores oxygen for aerobic respiration
● Many mitochondria → high rate of aerobic respiration
● Many capillaries → supply high conc. of oxygen / glucose for aerobic respiration and to prevent build-up of lactic acid causing muscle fatigue
60
What are the general properties of a fast twitch muscle?
● Specialised for brief, intensive contractions (eg. sprinting)
● Obtain ATP mostly from anaerobic respiration → release energy quickly
● Fatigues quickly due to high lactate conc
61
Where are fast twitch muscles located?
● High proportion in muscles used for fast movement eg. biceps, eyelids
● Legs of sprinters
62
What is the structure of a fast twitch muscle?
● Low levels of myoglobin
● Lots of glycogen → hydrolysed to provide glucose for glycolysis / anaerobic respiration which is inefficient so large quantities of glucose required
● High conc. of enzymes involved in anaerobic respiration (in cytoplasm)
● Store phosphocreatine
63
Describe homeostasis in mammals
● Maintenance of a stable internal environment within restricted limits
● By physiological control systems (normally involve negative feedback)
64
Explain the importance of maintaining stable core temperature
● If temperature is too high:
○ Hydrogen bonds in tertiary structure of enzymes break
○ Enzymes denature; active sites change shape and substrates can’t bind
○ So fewer enzyme-substrate complexes
● If temperature is too low:
○ Not enough kinetic energy so fewer enzyme-substrate complexes
65
Explain the importance of maintaining stable blood pH
● Above or below optimal pH, ionic / hydrogen bonds in tertiary structure break
● Enzymes denature; active sites change shape and substrates can’t bind
● So fewer enzyme substrate complexes
66
Explain the importance of maintaining stable blood glucose concentration
Too low (hypoglycaemia)
● Not enough glucose (respiratory substrate) for respiration
● So less ATP produced
● Active transport etc. can’t happen → cell death
Too high (hyperglycaemia)
● Water potential of blood decreases
● Water lost from tissue to blood via osmosis
● Kidneys can’t absorb all glucose → more water lost in urine causing dehydration
67
Describe the role of negative feedback in homeostasis
1. Receptors detect change from optimum
2. Effectors respond to counteract change
3. Returning levels to optimum / normal
68
Explain the importance of conditions being controlled by separate
mechanisms involving negative feedback
● Departures in different directions from the original state can all be controlled / reversed
● Giving a greater degree of control (over changes in internal environment)
68
Describe positive feedback
1. Receptors detect change from normal
2. Effectors respond to amplify change
3. Producing a greater deviation from normal
68
Describe the role of the liver in glycogenesis,
glycogenolysis and gluconeogenesis
Glycogenesis; Converts glucose → glycogen
Glycogenolysis; Converts glycogen → glucose
Gluconeogenesis; Converts amino acids and/or glycerol → glucose
68
Describe the factors that influence blood glucose concentration
● Consumption of carbohydrates → glucose absorbed into blood
● Rate of respiration of glucose - eg. increases during exercise due to muscle contraction
68
Explain the action of insulin in decreasing blood glucose concentration
● Attaches to specific receptors on cell surface membranes of target cells eg. liver / muscles
1. This causes more glucose channel proteins to join cell surface membrane
○ Increasing permeability to glucose
○ So more glucose can enter cell by facilitated diffusion
2. This also activates enzymes involved in conversion of glucose to glycogen (glycogenesis)
○ Lowering glucose concentration in cells, creating a concentration gradient
○ So glucose enters cell by facilitated diffusion
68
Explain the action of glucagon in increasing blood glucose concentration
Alpha cells in islets of Langerhans in pancreas detect blood glucose concentration is too low → secrete glucagon:
● Attaches to specific receptors on cell surface membranes of target cells eg. liver
1. Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis)
2. Activates enzymes involved in conversion of glycerol / amino acids to glucose (gluconeogenesis)
● This establishes a concentration gradient → glucose enters blood by facilitated diffusion
69
Explain the role of adrenaline in increasing blood glucose concentration
● Attaches to specific receptors on cell surface membranes of target cells eg. liver
● Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis)
● This establishes a concentration gradient → glucose enters blood by facilitated diffusion
69
Suggest an advantage of the second messenger model
● Amplifies signal from hormone
● As each hormone can stimulate production of many molecules of second messenger (cAMP)
● Which can in turn activate many enzymes for rapid increase in glucose
69
Describe the second messenger model of adrenaline and glucagon action
1. Activates enzyme adenylate cyclase (changes shape)
2. Which converts many ATP to many cyclic AMP (cAMP)
3. cAMP acts as the second messenger → activates protein kinase enzymes
4. Protein kinases activate enzymes to break down glycogen to glucose
70
What is the cause for type 1 diabetes?
● Key point = β cells in islets of langerhans in pancreas produce insufficient insulin
● Normally develops in childhood due to an autoimmune response destroying β cells of Islets of Langerhans
71
What is the cause for type 2 diabetes?
● Key point = receptor (faulty) loses responsiveness / sensitivity to insulin (but insulin still produced)
● So fewer glucose transport proteins → less uptake of glucose → less conversion of glucose to glycogen
● Risk factor = obesity
72
Describe how of type I diabetes can be controlled
● Injections of insulin
● Blood glucose concentration monitored with biosensors; dose of insulin matched to glucose intake
● Eat regularly and control carbohydrate intake eg. those that are broken down / absorbed slower
○ To avoid sudden rise in glucose
73
Suggest why insulin can’t be taken as a tablet by mouth
● Insulin is a protein
● Would be hydrolysed by endopeptidases / exopeptidases
74
Describe how of type II diabetes can be controlled
● Not normally treated with insulin injections but may use drugs which target
insulin receptors to increase their sensitivity
○ To increase glucose uptake by cells / tissues
● Reduce sugar intake (carbohydrates) / low glycaemic index → less absorbed
● Reduce fat intake → less glycerol converted to glucose
● More (regular) exercise → uses glucose / fats by increasing respiration
● Lose weight → increased sensitivity of receptors to insulin
75
Describe how you can evaluate the positions of health advisers and the food
industry in relation to the increased incidence of type II diabetes
● Health advisers aim - reduce risk of type II diabetes due to health problems caused (eg. kidney failure)
○ So need to reduce obesity as it is a risk factor
● Food industry aim - maximise profit
76
Describe the structure of a nephron
● Nephron = basic structural and functional unit of the kidney (millions in the kidney)
● Associated with each nephron are a network of blood vessels
77
What is the role of the Bowman’s / renal capsule?
Formation of glomerular filtrate (ultrafiltration)
78
What is the role of the Proximal convoluted tubule?
Reabsorption of water and glucose (selective reabsorption)
79
What is the role of the loop of henle?
Maintenance of a gradient of sodium ions in the medulla
80
What is the role for the . Distal convoluted tubule?
Reabsorption of water (permeability controlled by ADH)
81
what is the role of the collecting duct?
Reabsorption of water (permeability controlled by ADH)
82
Describe the formation of glomerular filtrate
1. High hydrostatic pressure in glomerulus
○ As diameter of afferent arteriole (in) is wider than efferent arteriole (out)
2. Small substances eg. water, glucose, ions, urea forced into glomerular filtrate, filtered by:
a. Pores / fenestrations between capillary endothelial cells
b. Capillary basement membrane
c. Podocytes
3. Large proteins / blood cells remain in blood
83
Describe the reabsorption of glucose by the proximal convoluted tubule
1. Na+ actively transported out of epithelial cells to capillary
2. Na+ moves by facilitated diffusion into epithelial cells down a concentration gradient, bringing glucose against its concentration gradient
3. Glucose moves into capillary by facilitated diffusion down its concentration gradient
84
Describe the reabsorption of water by the proximal convoluted tubule
● Glucose etc. in capillaries lower water potential
● Water moves by osmosis down a water potential gradient
85
Describe and explain how features of the cells in the PCT allow the rapid
reabsorption of glucose into the blood
● Microvilli / folded cell-surface membrane → provides a large surface area
● Many channel / carrier proteins → for facilitated diffusion / co-transport
● Many carrier proteins → for active transport
● Many mitochondria → produce ATP for active transport
● Many ribosomes → produce carrier / channel proteins
86
Suggest why glucose is found in the urine of an untreated diabetic person
● Blood glucose concentration is too high so not all glucose is reabsorbed at the PCT
● As glucose carrier / cotransporter proteins are saturated / working at maximum rate
87
Explain the importance of maintaining a gradient of sodium ions in the
medulla (concentration increases further down)
● So water potential decreases down the medulla (compared to filtrate in collecting duct)
● So a water potential gradient is maintained between the collecting duct and medulla
● To maximise reabsorption of water by osmosis from filtrate
88
Describe the role of the loop of Henle in maintaining a gradient of sodium
ions in the medulla
1. In the ascending limb:
○ Na+ actively transported out (so filtrate concentration decreases)
○ Water remains as ascending limb is impermeable to water
○ This increases concentration of Na+ in the medulla, lowering water potential
2. In the descending limb:
○ Water moves out by osmosis then reabsorbed by capillaries (so filtrate concentration increases)
○ Na+ 'recycled’ → diffuses back in
89
Suggest why animals needing to conserve water have long loops of Henle
(thick medulla)
● More Na+ moved out → Na+ gradient is maintained for longer in medulla / higher Na+ concentration
● So water potential gradient is maintained for longer
● So more water can be reabsorbed from collecting duct by osmosis
90
Describe the reabsorption of water by the distal convoluted tubule and
collecting ducts
● Water moves out of distal convoluted tubule & collecting duct by osmosis down a water potential gradient
● Controlled by ADH which increases their permeability
91
What is osmoregulation?
Control of water potential of the blood (by negative feedback)
92
Describe the role of the hypothalamus in osmoregulation
1. Contains osmoreceptors which detect increase OR decrease in blood water potential
2. Produces more ADH when water potential is low OR less ADH when water potential is high
93
Describe the role of the posterior pituitary gland in osmoregulation
Secretes (more / less) ADH into blood due to signals from the hypothalamus
94
Describe the role of antidiuretic hormone (ADH) in osmoregulation
1. Attaches to receptors on collecting duct (and distal convoluted tubule)
2. Stimulating addition of channel proteins (aquaporins) into cell-surface membranes
3. So increases permeability of cells of collecting duct and DCT to water
4. So increases water reabsorption from collecting duct / DCT (back into blood) by osmosis
5. So decreases volume and increases concentration of urine produced
