Unit 6 Flashcards

1
Q

Stimulus

A

A change in an organism’s internal or external environment.

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2
Q

Why is it important for organisms to respond to stimuli?

A

Increased chance of survival.

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3
Q

Tropism

A

-Growth of a plant in response to a directional stimulus.
-Positive tropism- towards a stimulus.
-Negative tropism- away from a stimulus.

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4
Q

Role of growth factors in flowering plants

A

-Specific growth factors move from growing regions to tips of roots or shoots.
-They regulate growth in response to directional stimuli.

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5
Q

How indoleacetic acid (IAA) affects cells in roots and shoots?

A

-In shoots, high conc of IAA stimulates cell elongation.
-In roots, high concentrations of IAA inhibit cell elongation.

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6
Q

Gravitropism in flowering plants

A

-Cells in tips of roots produce IAA.
-IAA diffuses down root.
-IAA moves to lower side of root so concentration increases.
-In the roots, IAA inhibits cell elongation.
-Upper cell elongates and roots bend towards gravity.

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7
Q

Phototropism in flowering plants

A

-Cells in tips of shoot produce IAA.
-IAA diffuses down shoot.
-IAA moves to shaded side of shoot so concentration increases.
-In the shoots, IAA stimulates cell elongation.
-Cells grow and bend towards the light.

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8
Q

Taxes

A

-Tactic response.
-Directional response.
-Movement towards or away from a directional stimulus.

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9
Q

Kinesis

A

-Kinetic response.
-Non-directional response.
-Speed of movement or rate of direction change changes in response to a non-directional stimulus.
-Depending on intensity of stimulus.

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10
Q

Basic structure of Pacinian corpuscle

A

-Lamaellae (layers of connective tissue).
-Sensory neurone ending.
-Sensory neurone axon.
-Gel.
-Myelin sheath.
-Stretch mediated sodium ion channel.

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11
Q

How is a generator potential established in a Pacinian corpuscle?

A

-Mechanical stimulus- pressure deforms lamellar and stretch mediated sodium channels open.
-Na+ diffuse into sensory neurone.
-Greater pressure causes more Na+ channels to open and more Na+ to enter.
-This causes depolarisation which leads to a generator potential.
-If generator potential reaches threshold, it triggers an action potential.

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12
Q

What does the Pacinian corpuscle illustrate?

A

-Receptors respond only to specific stimuli.
-Stimulation of a receptor leads to the establishment of a generator potential.
-When threshold is reached, action potential sent (all or nothing principle).

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13
Q

Rods sensitivity to light intensity

A

-Several rods connected to a single neurone.
-Spatial summation to reach threshold (as enough neurotransmitter released) to generate an action potential.

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14
Q

Cones sensitivity to light

A

-Each cone connected to one single neurone.
-No spatial summation.

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15
Q

Rod cells visual acuity

A

-Low visual acuity.
-Several rods connected to a single neurone.
-Several rods send a single set of impulses to brain (can’t distinguish between separate sources of light).

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16
Q

Cone cells visual acuity

A

-High visual acuity.
-Each cone connected to a single neurone.
-Cones send separate impulses to brain (can distinguish between 2 separate sources).

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17
Q

Rod cells sensitivity to colour

A

-1 type of pigment
-Monochromatic vision.

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18
Q

Cone cells sensitivity to colour

A

-3 types of cones- red-, green- and blue-sensitive.
-Different optical pigments- absorb different wavelengths.
-Stimulating different combinations of cones gives range of colour perception.

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19
Q

Cardiac muscle is myogenic?

A

-It can contract and relax without receiving electrical impulses from nerves.

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20
Q

Nodes on the heart

A

-Sinoatrial Node (SAN)
-Atrioventricular node (AVN)
-Purkyne tissue
-Bundle of His

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21
Q

Myogenic stimulation of the heart

A

-Sinoatrial node (SAN) acts as a pacemaker- releases regular waves of electrical activity across atria.
-Causes atria to contract simultaneously.
-Non-conducting tissue between atria/ ventricles prevents impulse passing directly to ventricles.
-Preventing immediate contraction of ventricles.
-Waves of electrical activity reach atrioventricular node (AVN) which delays impulse.
-Allowing atria to fully contract and empty before ventricles contract.
-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.

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22
Q

Where are chemoreceptors and pressure receptors located?

A

In the aorta and carotid arteries

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23
Q

Rise in blood pressure, rise in pH

A

-Baroreceptors detect rise in bp and chemoreceptors detect blood fall in blood CO2 conc or rise in blood pH.
-Send impulses to medulla oblonganta/ cardiac control centre.
-Sends more frequent impulses to SAN along parasympathetic neurones.
-So less frequent impulses sent from SAN to AVN.
-Cardiac muscle contracts less frequently.
-Heart rate decreases.

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24
Q

Fall in blood pressure, fall in blood pH

A

-Baroreceptors detect fall in bp and chemoreceptors detect blood rise in blood CO2 conc or fall in blood pH.
-Send impulses to medulla oblonganta/ cardiac control centre.
-Sends more frequent impulses to SAN along sympathetic neurones.
-So more frequent impulses sent from SAN to AVN.
-Cardiac muscle contracts more frequently.
-Heart rate increases.

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25
Structure of a myelinated motor neurone
-Dendrites -Cell body (soma) -Axon -Myelin sheath -Node of ranvier
26
Resting potential
Inside of the axon has a negative charge relative to the outside.
27
How is resting potential established?
-Na+/K+ pump actively transports 3Na out of the axon and 2K into the axon. -Creates an electrochemical gradient. -Higher K+ conc inside and higher Na+ conc outside. -Differential membrane permeability. -More permeable to K+- moved out by FD. -Less permeable to Na+ (closed channels).
28
Stimulus
-Na+ channels open, membrane permeability to Na+ increases. -Na+ diffuse into the axon down electrochemical gradient (causes depolarisation).
29
Depolarisation
-If threshold potential is reached, an action potential is triggered. -As more voltage-gated Na+ channels open (positive feedback effect). -More Na+ diffuse in rapidly.
30
Repolarisation
-Voltage-gated Na+ channels close. -Voltage-gated K+ channels open, K+ diffuse out of axon.
31
Hyperpolarisation
-K+ channels slow to close so there's a slight overshoot. -Too many K+ diffuse out. -Na+/K+ pump restore resting potential.
32
Action potential graph
Draw and label.
33
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 increase frequency of action potentials.
34
Action potential- non-myelinated axon
-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.
35
Action potential- myelinated axon
-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 the whole length of axon.
36
Damage to the myelin- slow/ jerky movements
-Less saltatory conduction- depolarisation occurs along whole length of axon. -Nerve impulses take longer to reach neuromuscular junction, delay in muscle contraction. -Ions may pass to other neurones. -Causing wrong muscle fibres to contract.
37
Refractory period
-Time taken to resture axon to resting potential when no further action potential can be generated. -As Na+ channels are closed/ inactive/ will not open.
38
Importance of the refractory period
-Ensures discrete impulses are produced- AP don't overlap. -Limits frequency of impulse transmission at a certain intensity- prevents over reaction to stimulus. -But only up to a certain intensity. -Also ensures action potentials travel in one direction- can't be propagated in a refractory region. -(In the second half of refractory period, an AP can be produced but requires greater stimulation to reach threshold).
39
Factors that affect speed of conductance
-Myelination -Axon diameter -Temperature
40
Myelination
-Depolarisation at Nodes of Ranvier only- saltatory conduction. -Impulse doesn't travel/ depolarise whole length of axon.
41
Axon diameter
-Bigger diameter means less resistance to flow of ions in cytoplasm.
42
Temperature
-Increases rate of diffusion of Na+ and K+ as more KE. -But proteins/ enzymes could denature at a certain temp.
43
Cholinergic Synapse
-A gap in between two neurones that uses the neurotransmitter acetylcholine (ACh). -Draw it!!!
44
Describe transmission across a cholinergic synapse
-Depolarisation of pre-synaptic membrane causing opening of voltage-gated Ca2+ channel. -Ca2+ diffuse into pre-synaptic knob. -Causing vesicles containing ACh to move and fuse with pre-synaptic membrane. -Releasing ACh into the synaptic cleft by exocytosis. -ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane. -Causing Ligand-gated sodium channels to open. -Na+ diffuse into post-synaptic knob causing depolarisation. -If threshold is met, AP is initiated.
45
What happens to acetylcholine after synaptic transmission?
-It is hydrolysed by acetylcholinesterase. -Into acetate and choline. -Products are reabsorbed by the presynaptic neurone. -To stop overstimulation- if not removed it would keep binding to receptors causing depolarisation.
46
Unidirectional nerve impulses
-Neurotransmitter only made in pre-synaptic neurone. -Receptors only on post-synaptic membrane.
47
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 AP.
48
Spatial summation
-Many pre-synaptic neurones hare one synaptic cleft. -Collectively release sufficient neurotransmitter to reach threshold to trigger an action potential.
49
Temporal summation
-One pre-synaptic neurone releases neurotransmitter many times over a short time. -Sufficient neurotransmitter to reach threshold to trigger an action potential.
50
Inhibition by inhibitory synapses
-Inhibitory neurotransmitters hyperpolarise postsynaptic membranes as: -Cl- channels open- Cl- diffuses in. -K+ channels open- K+ diffuses out. -This means the inside of axon has a more negative charge relation to outside (below resting potential). -More Na+ required to enter for depolarisation. -Reduces likelihood of threshold being met and AP being established.
51
Structure of a neuromuscular junction
-Receptors are on muscle fibre sarcolemma instead of postsynaptic membrane and there are more. -Muscle fibre forms clefts to store enzyme to break down neurotransmitter.
52
Compare transmission across cholinergic and neuromuscular junctions.
-Neurone to neurone vs motor neurone to muscle. -Excitatory or inhibitory vs always excitatory. -AP initiated in postsynaptic neurone vs AP propagates along sarcolemma down T tubules.
53
Effect of drugs on a synapse
-Some drugs stimulate the nervous system, leading to more action potentials. -Similar shape to neurotransmitter. -Stimulate release of more neurotransmitter. -Inhibit enzyme that breaks down neurotransmitter- Na+ contains to enter. -Some drugs inhibit the nervous system, leading to fewer action potentials. -Inhibit release of neurotransmitter. -Block receptors by mimicking shape of neurotransmitter.
54
How muscles work?
-Work in antagonistic pairs and pull in opposite directions. -One muscle contracts (agonist)- pulling on bone- producing force. -One muscle relaxes (antagonist). -Skeleton is incompressible so muscles transmit force to bone.
55
Gross structure of skeletal muscle
-Made of many bundles of muscle fibres (cells) packaged together. -Attached to bones by tendons.
56
Microscopic structure of skeletal muscle
-Muscle fibres contain: -Sarcolemma- cell membrane which folds inwards to form transverse T tubules. -Sarcoplasm- cytoplasm. -Multiple nuclei. -Many myofibrils. -Sarcoplasmic reticulum- endoplasmic reticulum. -Many mitochondria.
57
Ultrastructure of a myofibril
-Two types of protein filaments arranged in parallel- myosin (thick) and actin (thin). -Arranged in functional units called sarcomeres. -Ends- Z line -Middle- M line -H zone- contains only myosin.
58
Banding pattern seen in myofibrils
-I-band- light bands containing only thin actin filaments. -A-band- dark bands containing thick myosin filaments. -H zone contains only myosin. -Darkest region contains overlapping actin and myosin.
59
Evidence for sliding filament theory
-Myosin heads slide actin along myosin causing the sarcomeres to contract. -Stimultaneous contraction of many sarcomeres causes myofibrils and muscle fibres to contract. -When sarcomeres contract: -H zones get shorter -I band get shorter -A band stays the same -Z lines get closer
60
Muscle contraction mechanism
-Depolarisation spreads down sarcolemma via T tubules causing Ca2+ release from sarcoplasmic reticulum which diffuse to myofibrils. -Ca2+ bind to tropomyosin causing it to move which exposes binding sites on actin. -Allowing myosin head, with ADP attached, to bind to binding sites on actin which forms an actinmyosin crossbridge. -Myosin heads change angle, pulling actin actin along myosin (ADP released), using energy from ATP hydrolysis. -New ATP binds to myosin head causing it to detach from binding site. -Hydrolysis of ATP by ATP(hydrol)ase (activated by Ca2+) releases energy for myosin heads to return to original position. -Myosin reattaches to a different binding site further along actin. Process is repreated as long as Ca2+ concentration is high.
61
During muscle relaxation
-Ca2+ actively transported back into the endoplasmic reticulum using energy from ATP. -Tropomyosin moves back to block myosin binding site on actin again. -So no more actinmyosin crossbridges can form.
62
Role of phosphocreatine
-Source of 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.
63
Slow twitch skeletal muscle fibres
General properties -Specialised for slow, sustained contractions- long distance running, posture. -Produce more ATP slowly from aerobic respiration. -Fatigues slowly. Location -High proportion in muscles used for posture- back, calves. -Legs of long distance runners. Structure -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.
64
Fast twitch skeletal muscle fibres
General properties -Specialised for brief, intensive contractions- sprinting. -Produces less ATP rapidly from anaerobic respiration. -Fatigues quickly due to high lactate conc. Location -High proportion in muscles used for fast movement- biceps, eyelids. -Legs of sprinters. Structure -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.
65
Homeostasis in mammals
-Maintenance of a stable internal environment within restricted limits. -By physiological control systems- normally involve negative feedback.
66
Importance of maintaining stable core temperature
-If temp 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 temp is too low -Not enough kinetic energy so fewer enzyme-substrate complexes.
67
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.
68
Low blood glucose conc (hypoglycaemia)
-Not enough glucose (respiratory substrate) for respiration. -So less ATP produced. -Active transport- can't happen- cell death.
69
High blood glucose conc (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.
70
Role of negative feedback in homeostasis
-Receptors detect change from optimum. -Effectors respond to counteract change. -Returning levels to optimum/normal.
71
Importance of conditions being controlled by 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 envrionment.
72
Positive feedback
-Receptors detect change from normal. -Effectors respond to amplify change. -Producing a greater deviation from normal.
73
Factors that influence blood glucose concentration
-Consumption of carbohydrates- glucose absorbed into blood. -Rate of respiration of glucose.
74
Glycogenesis
Converts glycose to glycogen
75
Glycogenolysis
Converts glycogen to glucose
76
Gluconeogenesis
Converts amino acids and glycerol into glucose.
77
Action of insulin
-Beta cells in islets of Langerhans in pancreas detect blood glucose concentration is too high- secretes insulin. -Attaches to specific receptors on cell surface membranes of target cells. -Causes more glucose channel proteins to join cell surface membrane. -Increasing permeability to glucose. -So more glucose can enter cell by facilitated diffusion. -Activates enzymes involved in conversion of glucose to glycogen. -Lowering glucose concentration in cells, creating a concentration gradient. -Glucose enters cell by facilitated diffusion.
78
Action of glucagon
-Alpha cells of islets of Langerhans in pancreas detect low blood glucose concentration- secretes glucagon. -Attaches to specific receptors on cell surface membranes of target cells. -Activates enzymes involved in hydrolysis of glycogen to glucose. -Activates enzymes involved in conversion of glycerol/ amino acids to glucose. -Establishes a conc gradient- glucose enters blood by facilitated diffusion.
79
Role of adrenaline
-Adrenal glands secrete adrenaline. -Attaches to specific receptors on cell surface membranes of target cells. -Activates enzymes involved in hydrolysis of glycogen to glucose. -Establishes a concentration gradient- glucose enters blood by facilitated diffusion.
80
Second messenger model
-Adrenaline/ glucagon attach to specific receptors on cell membrane -Activates enzyme adenylate cyclase (changes shape). -Which converts many ATP to many cyclic AMP (cAMP). -cAMP acts as the second messenger- activates protein kinase enzymes. -Protein kinases activate enzymes to break down glycogen to glucose.
81
Advantage of 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.
82
Causes of type 1 diabetes
-Beta cells in islets of langerhans in pancreas produce insufficient insulin. -Normally develops in childhood due to an autoimmune response destroying beta cells.
83
Causes of type 2 diabetes
-Receptor loses responsiveness/ sensitivity to insulin. -So fewer glucose transport proteins- less uptake of glucose- less conversion of glucose to glycogen. -Risk factor- obesity.
84
How can type 1 diabetes be controlled?
-Injections of insulin as pancreas doesn't produce enough. -Blood glucose conc monitored with biosensors, dose pf insulin matched to glucose intake. -Eat regularly and control carbohydrate intake. -Avoid sudden rise in glucose.
85
Why insulin can't be taken as a tablet?
-Insulin is a protein. -Would be hydrolysed by endopeptidases/ exopeptidases.
86
How can type 2 diabetes 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- low glycaemic index- less absorbed. -Reduce fat intake- less glycerol converted to glucose. -More exercise- uses glucose/ fats by increasing respiration. -Lose weight- increased sensitivity of receptors to insulin.
87
Structure of the nephron
-Nephron- basic structural and functional unit of the kidney- millions in the kidney. -Associated with each nephron are a network of blood vessels.
88
Bowman's/ renal capsule
Formation of glomerular filtrate (ultrafiltration)
89
Proximal convoluted tubule
Reabsorption of water and glucose- selective reabsorption
89
Loop of Henle
Maintenance of a gradient of sodium ions in the medulla.
90
Distal convoluted tubule/ collecting duct
Reabsorption of water- permeability controlled by ADH.
91
Formation of glomerular filtrate
-High hydrostatic pressure in glomerulus as afferent arteriole (in) is wider than efferent arteriole (out). -Small substances (water, glucose, ions, urea) forced out into glomerular filtrate. -It is filtered by- pores/ fenestrations between capillary endothelial cells, capillary basement membrane, podocytes. -Large proteins/ blood cells remain in blood.
92
Reabsorption of glucose by the proximal convoluted tubule
-Na+ actively transported out of epithelial cells to capillary. -Na+ moves by facilitated diffusion into epithelial cells down a concentration gradient, bringing glucose against its concentration gradient. -Glucose moves into capillary by facilitated diffusion down its concentration gradient.
93
Reabsorption of water by the proximal convoluted tubule
-Glucose etc. in capillaries lower water potential. -Water moves by osmosis down a water potential gradient.
94
Features of the cells in the PCT which allow the rapid reabsorption of glucose
-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.
95
Diabetic person- glucose in urine
-Blood glucose concentration is too high so noy all glucose is reabsorbed at the PCT. -As glucose carrier/ cotransporter proteins are saturated, working at maximum rate.
96
Importance of maintaining a gradient of sodium ions in medulla
-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.
97
Role of loop of Henle in maintaining a gradient of sodium ions in the medulla
Ascending limb- -Na+ actively transported out (so filtrate conc decreases). -Water remains as ascending limb is impermeable to water. -This increases concentration of Na+ in the medulla, lowering water potential. Descending limb- -Water moves out by osmosis then reabsorbed by capillaries (so filtrate conc increases). -Na+ 'recycled'- diffuses back in.
98
Why animals have long loops of Henle?
-More Na+ moved out- Na+ gradient is maintained for longer in medulla/ higher Na+ conc. -So water potential gradient is maintained for longer. -So more water can be reabsorbed from collecting duct by osmosis.
99
Reabsorption of water by DCT and collecting duct
-Water moves out of DCT and collecting duct by osmosis down a water potential gradient. -Controlled by ADH which increases their permeability.
100
Osmoregulation
Control of water potential of the blood- by negative feedback.
101
Role of hypothalamus in osmoregulation
-Contains osmoreceptors which detect increase or decrease in blood water potential. -Produces more ADH when water potential is low or less ADH when water potential is high.
102
Role of posterior pituitary gland in osmoregulation
Secretes more/less ADH into blood due to signals from the hypothalamus.
103
Role of antidiuretic hormone (ADH) in osmoregulation
-Attaches to receptors on collecting duct and DCT. -Stimulating addition of channel proteins (aquaporins) into cell-surface membranes. -So increases permeability permeability of cells of collecting duct and DCT to water. -So increases water reabsorption from collecting/ DCT (back into blood) by osmosis. -So decreases volume and increases concentration of urine produced.