Topic 6 - Organisms Respond To Changes In Their Internal And External Environments Flashcards

(82 cards)

1
Q

Responses for survival

A

A stimulus is a detectable change in the environment.
These changes can be detected by receptors.
Organisms increase chance of survival by responding to stimuli via different response mechanisms.

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2
Q

Tropism

A

When plants respond, via growth, to stimuli
Can be positive or negative, growing towards or away from stimulus
Controlled by specific growth factors (E.g. indoleacetic acid (IAA)
IAA - type of auxin, controls cell elongation in shoots and inhibits growth of cells in roots, made in tip or roots and shoots but can diffuse to other cells in

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3
Q

Positive Phototropism

A

Shoots:
- light needed for LDR in photosynthesis, so plants grow and bend towards light (positive phototropism)
1. Shoot tip cells produced IAA, causing cell elongation
2. IAA diffuses to other cells
3. If there is unilateral light, IAA diffuses towards shaded side of shoot - results in higher concentration of IAA there
4. Cells on shaded side elongate more and results in plant bending towards light source

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4
Q

Negative phototropism

A

Roots:
- don’t photosynthesise so don’t require light
- must anchor plant deep in the so8l
- high concentration of IAA inhibits cell elongation - causes roots cells to elongate more on lighter side and so root bends away from light.

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5
Q

Negative Gravitropism

A

Shoots:
- IAA diffuses from upper side to lower side of shoot
- if plant is vertical, causes plant cells to elongate and plant grows upwards
- if plant on its side, cause shoot to bend upwards

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6
Q

Positive Gravitropism

A

Roots:
- IAA moves to lower side of roots - upper side elongates and root bends down towards gravity and anchors plant

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7
Q

Reflexes

A

Reflex - rapid automatic response to protect animals from danger
Reflex arc made of up three neurones - sensory, relay, motor
Rapid - only two synapses

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8
Q

Simple Responses - Taxes and Kinesis

A

Keep organisms within favourable conditions of their environment (light, moisture, chemicals)
Taxes - move entire body towards favourable stimulus (positive taxis) or away from unfavourable stimulus (negative taxis)
Kinesis - changes speed of movement and rate it changes direction

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9
Q

Receptors

A

Detect stimuli
Each receptor responds only to specific stimuli - stimulation leads to establishment of an action potential which can cause a response
Three receptors to know:
- pacinian corpuscle
- rods
- cones

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10
Q

Pacinian corpuscle

A
  • deep in skin, mainly in fingers and feet
  • sensory neurons in pacinian corpuscle has special channel proteins in plasma membrane
  • membranes have stretch-mediated sodium channels - open and allow Na+ to enter sensory neurons when stretched and deformed.
  • when pressure is applied it deforms neurone plasma membrane, stenches and widens NA+ channels so it can diffuse in - leads to action potential
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11
Q

Rods Cells

A

Process images in black and white
To create action potential, pigment of rod cells (rhodopsin) must be broken down into light energy
Detect light of very low intensity as many rod cells connect to one sensory neurone (retinal convergence) - means brain cannot distinguish between separate sources of light that stimulated it - low visual acuity

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12
Q

Cone Cells

A

Process images in colour
Three types that contain different types of iodopsin pigment (red, green, blue) which all absorb different wavelengths of light
Iodopsin broken down if high light intensity - action potentials can only be generated with enough light
One cone cell connects to a bipolar cell - cones can only respond to high light intensity - why we can’t see colour in the dark
Connected to a bipolar cell - rain distinguish between separate sources of light - high visual acuity

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13
Q

Distribution of Rods and Cones

A

Uneven distribution in retina
Light focused by lens on the fovea - receive highest light intensity
Most cone cells located near fovea
Rod cells further away

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14
Q

Cardiac Muscle

A

Myogenic - it contracts on its own accord, but rate of contraction is controlled by wave of electrical activity (nervous system)

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15
Q

Sinoatrial Node (SAN)

A

Located in right atrium
Known as the pacemaker

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16
Q

Atrioventricular Node (AVN)

A

Located between right atrium and left ventricle within atria still

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17
Q

What tissues run down the septum

A

Bundle of His

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18
Q

What fibres are in the walls of the ventricles

A

Purkyne fibres

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19
Q

Control of Heart rate

A
  • SAN releases wave of depolarisation across the two atria, causing it to contract
  • AVN releases another wave of depolarisation when first wave reaches it.Non- conductive layer between atria and ventricles prevents wave of depolarisation travelling down to ventricles
  • instead, bundle of His, conducts the wave of depolarisation down the septum and the Purkyne fibres
  • as a result, apex and walls of ventricles contract - short delay before this happens whilst AVN transmits second waves of depolarisation - allows enough time for atria to pump all blood into ventricles
  • finally, the cells depolarise, and the cardiac muscle relaxes.
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20
Q

Medulla Oblongata

A

In brain
Controls heart rate via the autonomic nervous system
Two pats:
- a centre linked to SAN to increase heart rate via sympathetic nervous system - release waves of depolarisation more frequently
- another that decreases heart rate via parasympathetic nervous system - release waves of depolarisation less frequently

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21
Q

Homeostatic Control of Heart Rate

A

Heart rate changes in response to pH and blood pressure - stimuli detected by chemoreceptors and pressure receptors

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22
Q

Myelinated Motor Neurone

A

The cell body of the neurone contains the organelles found in a typical animal cell. Proteins and neurotransmitter chemicals are made here

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23
Q

Dendrites

A

Carry action potentials to surrounding cells

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24
Q

Axon

A

Conductive, long fibre
Carries nervous impulse along motor neurone

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25
Schwann Cells
Wrap around axon to form myelin sheath - lipid so doesn’t allow charged ions to pass through it Gaps between myelin sheath called nodes of Ranvier
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Resting Potential
Neurone not conducting an impulse - difference between electrical charge inside and outside of the neurone More positive ions (Na+ and K+) outside compared to inside - inside of neurone more negative
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Establishing a Resting Potential
Maintained by sodium-potassium pump, involving active transport and ATP Pump moves 2 K+ ions in and 3 Na+ ions out Creates electrochemical gradient - causes K+ to diffuse out and Na+ to diffuse in
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Action Potential
Neurone’s voltage increases beyond a set point from the resting potential - generates nervous impulse Increase in voltage, or depolarisation, is due to neurone membrane becoming more permeable to Na+
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All-or-nothing principle
If depolarisation doesn’t exceed -55mV no action potential or impulse is produced (Nothing) Any stimulus that does exceed depolarisation of -55mV will always peak at the same max voltage. (All) Bigger stimuli increase frequency of action potentials Makes sure animals only respond to large enough stimuli
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Refractory Period
After action potential is generated, membrane enters refractory period when it can’t be stimulated because sodium channels are recovering and can’t be opened.
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Importance of Refractory Period
- ensures that discrete impulses are produced - action potentials can’t be generated one after another so this makes sure that each is separate - ensures that action potentials travel in one direction - stops action potential from spreading out in two directions which would prevent a response - limits number of impulse transmission - prevent over reaction to stimulus
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Factors affecting speed of conductance
Myleination and saltatory conduction Axon diameter Temperature
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Myelination and Saltatory conduction
Action potential jumps from node to node (saltatory conduction), which means action potentials travels along the axon faster
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Axon diameter
Wider diameter increases speed of conductance - less leakage of ions and therefore action potentials travels faster
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Temperature
Higher temperature increases speed of conductance because: - ions diffuse faster - enzymes involved in respiration work faster - more ATP for active transport in the sodium-potassium pump
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Synapses
Gaps between end of axon of one neurone and the dendrite of another Action potentials transmitted as neurotransmitters that diffuse across the synapse
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Function of synapse
- action potential arrives at synaptic knob. Depolarisation of knob leads to opening of Ca2+ channels and Ca2+ diffuses into synaptic knob - vesicles containing neurotransmitters move towards and fuse with Presynaptic membrane. Neurotransmitters released to synaptic gap. - neurotransmitters diffuse down concentration gradient across gap to post synaptic membrane. Neurotransmitters binds to receptors on surface of post synaptic membrane - Na+ ion channels on post membrane open and Na+ diffuse in, if enough neurotransmitters, then enough Na+ diffuse in, above threshold, and post-synaptic neuron becomes depolarised - Neurotransmitters degraded and released from receptor, the Na+ channel close and the post neuron reestablishes resting potential. Neurotransmitters transported back to Presynaptic neuron where they are recycled
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Neurotransmitter in Cholinergic Synapse
Acetylcholine Enzyme breaks acetylcholine back into Choline+Acetate
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Summation
Rapid build-up of neurotransmitters in synapse to help generate an action potential - spatial summation - temporal summation
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Spatial Summation
Many different neurones collectively trigger action potential by combining neurotransmitters they release to exceed threshold value
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Temporal Summation
One neurone releases neurotransmitter repeatedly over short period of time to add up to enough to exceed threshold value
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Inhibitory Synapse
- cause chloride ions to move into postsynaptic neurone and potassium ions to move out - makes membranes potential decrease to -80mV, hyperpolarisation - action potential unlikely
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Neuromuscular Junction
Synapse that occurs between a motor neurone and a muscle
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Similarity between Neuromuscular Junction and Cholinergic Synapse
Unidirectional due to neurotransmitter receptors only being on post synaptic membrane
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Differences between Neuromuscular Junction (NJ) and Cholinergic Synapse (CS)
- NJ only excitatory, CS both excitatory and inhibitory - NJ connects motor neurone to muscles, CS connects two neurones - NJ is end point for action potential, CS a new action potential is generated in next neurone - NJ acetylcholine binds to receptors on muscle fibre membranes, CS acetylcholine binds to receptors on Postsynaptic membrane of a neurone
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How do muscles act?
Muscles act in antagonistic pairs against an incompressible skeleton to create movement. Can be automatic as part of a reflex response or controlled conscious thought
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Myofibrils
Made up of fused cells that share nuclei and cytoplasm (sarcoplasm), and there is a high number of mitochondria Millions of myofibrils make up muscle fibres.
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Sarcomere
Two key proteins in myofibrils, myosin and actin, form a sarcomere
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Sliding Filament Theory
1. When an action potential reaches a muscle, it stimulates a response 2. Calcium ions enter and cause the protein tropomyosin to move and uncover the binding sites on actin 3. Whilst ADP is attached to myosin head, myosin heads to actin to form a cross-bridge 4. Angle created in cross-bridge creates tension - actin filament pulled and slides along the myosin. In doing so the ADP molecules are released. 5. ATP molecule binds to myosin head and cause shape to change - as a result it detaches from actin 6. Within sarcoplasm, enzyme ATPase which is activated by calcium ions, to hydrolyse ATP on myosin head into ADP and releases enough energy for myosin head to go back to original position 7. Entire process repeats continually whilst calcium ions remain Hugh and therefore muscle remains stimulated by nervous system
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ATP and Phosphocreatine
Active muscles need a high concentration of ATP The chemical phosphocreatine, which is stored in muscles, assists this by providing phosphate to regenerate ATP from ADP
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Difference in Structure between Slow and Fast twitch fibres
Slow-twitch fibres - contains large store of myoglobin, a rich blood supply and many mitochondria Fast-twitch fibres - thicker and more myosin filaments, large store of glycogen, a store of phosphocreatine to help make ATP from ADP, and a high concentration of enzymes involved in aerobic respiration
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Differences in Location between Slow and Fast twitch fibres
Slow-twitch fibres - calf muscles Fast-twitch fibres - biceps
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Differences in general properties between slow and fast twitch fibres
Slow-twitch fibres - contract slower and can respite aerobically for longer due to rich blood supply and myoglobin oxygen store. Muscles adapted for endurance work. Fast-twitch fibres - contract faster to provide short burst of powerful contraction. Muscles adapted for intense exercise like sprinting or weight lifting.
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Homeostasis
Homeostasis involves physiological control systems that maintain the internal environment within restriction limits. Important in maintaining - stable core temperature, stable blood pH in relation to enzyme activity
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Blood Glucose Concentration Changes
Increases - ingestion of food or drink containing carbohydrates Decreases - following exercise or if you have not eaten
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Pancreas Role in Blood Glucose Concentration
- Detects changes in blood glucose levels - Islets of Langerhans cells release insulin and glucagon to bring blood glucose back to normal
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Insulin Role in Blood Glucose Concentration
- released when blood glucose levels are too high. - causes a decrease in blood glucose levels
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Glucagon Role in Blood Glucose Concentration
- released when blood glucose levels are too low - causes increase in blood glucose levels
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Adrenaline Role in Blood Glucose Concentration
- released by adrenal glands when body anticipates danger - release results in more glucose being released from hydrolysis of glycogen in liver
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What happens when Blood Glucose level increases
1. Blood glucose levels increases 2. Detected by beta cells in the Islets of Langerhans (pancreas) 3. Beta cells release insulin 4. Liver cells become more permeable to glucose and enzymes activated to convert glucose to glycogen 5. Glucose removed from blood and stored as glycogen in cells 6. Normal blood glucose levels increases
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What happens when blood glucose levels decreases
1. Blood glucose levels decreases 2. Detected by alpha cells in Islets of Langerhans (pancreas) 3. Alpha cells release glucagon and Adrenal Gland release adrenaline 4. Second messenger model occurs to activate enzymes to hydrolyse glycogen 5. Glycogen hydrolysed to glucose and more glucose is released back into blood 6. Normal blood glucose levels
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How does Insulin decrease blood glucose levels
- attaching to receptors on surface of target cells - changes tertiary structure of channel proteins resulting in more glucose being absorbed by facilitated diffusion - more protein channels incorporated into cell membranes - more glucose absorbed from blood into cells - activating enzymes involved in conversion of glucose to glycogen - results in glycogenesis in liver
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How does glucagon increase blood glucose levels
- attaching to receptors on surfaces of target cells (liver cells) - when glucagon binds it causes protein to activate into adenylate cyclase and to convert ATP in molecule called cyclic AMP (cAMP). cAMP activates enzyme, protein kinase that can hydrolyse glycogen into glucose - activating enzymes involved in conversion of glycerol and amino acids into glucose
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Second Messenger Model
1. Glucagon binding to glucagon receptors 2. Once bound, causes change in shape to enzyme adenyl cyclase which activates it 3. Activated adenyl cyclase enzymes converts ATP into cyclic AMP (cAMP). cAMP is the second messenger model
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How does adrenaline increase blood glucose levels (second messenger model)
- adrenaline attaches to receptors on surface if target cells. Causes protein (G protein) to activate and convert ATP into cAMP. - cAMP activates enzyme that can hydrolyse glycogen into glucose - known as second messenger model of adrenaline and glucagon action, because the process results in formation of cAMP, which acts as a second messenger model
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Role of Liver
Glycogenesis - converting glucose into glycogen. Occurs in liver and is catalysed by enzymes Glycogenolysis - hydrolysis of glycogen to glucose. Occurs in liver due the second messenger model Gluconeogenesis - creating of glucose from other molecules such as amino acids and glycerol in the liver
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Type I diabetes
- unable to produce insulin - usually starts in childhood and could be the result of an autoimmune disease where beta cells are attacked - treatment involves injection of insulin
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Type II diabetes
- receptors on target cells lose responsiveness to insulin - usually develops in adults because of obesity and poor diet - controlled by regulating intake if carbs, increasing exercise and sometimes insulin injections
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Osmoregulation
- Controlling water potential of blood - hypertonic - blood with too low a water potential - hypotonic - blood with too high a water potential - crenation - too much water will leave cells and move into blood by osmosis. Cells will shrivel - lysis - too much water will move from blood into cells by osmosis. Cells will burst
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Hypertonic
- blood with too low a water potential - too much sweating, not drinking enough water, lots of ions in diet (lots of salt) Corrective mechanism - more water reabsorbed by osmosis into blood from the tubules of the nephrons. This means the urine is more concentrated as less water lost in the urine
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Hypotonic
- Blood with too high a water potential - drinking too much water, not enough salt in diet - Corrective mechanism - less water reabsorbed by osmosis into blood from the tubules of the nephrons. This means urine is more dilute and more water is lost in the urine.
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Structure of nephron
- long tubules surrounded by capillaries and there are around 1 million per kidney - osmoregulation occurs in nephrons in the kidneys - blood is filtered here to remove waste and selectively reabsorb useful substances back into the blood Structure: 1. Glomerulus - filters small solutes from the blood 2. Proximal Convoluted tubule - reabsorbed ions, water and nutrients, removes toxins and adjusts filtrate pH 3. Descending loop of Henle - aquaporins allow water to pass from filtrate into the interstitial fluid 4. Ascending loop of Henle - reabsorbed Na+ and Cl- from filtrate into interstitial fluid 5. Distal tube - selectively secretes and absorbs different ions to maintain blood pH and electrolyte balance 6. Collecting duct - reabsorbs solutes and water from filtrate
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Ultrafiltration
- occurs due to high hydrostatic pressure - water and small molecules are forced out of glomerulus capillaries into renal capsule
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Selective reabsorbtion
Occurs in proximal convoluted tubule
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Loop of Henle
Maintains sodium ion gradient so water can be reabsorbed into blood from the
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Distal convoluted tubule and Collecting duct to return
Water moves out of distal convoluted tubule and collecting duct to return to blood
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Collecting duct
Carries remaining liquid (urine) to the ureter
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Hypothalamus and posterior pituitary gland
- changes in water potential of blood are detected by osmoreceptors here - produces ADH - then moves to posterior pituitary and from here it is release into capillaries and into the blood
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Osmoreceptors
If water potential of blood is too low, water leaves the osmoreceptors by osmosis and they shrivel. This stimulates the hypothalamus to produce more of hormone ADH If water potential of blood is too high, water enters the osmoreceptors by osmosis. This stimulates the hypothalamus to produce less ADH
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ADH - Antidiuretic hormone
- causes increase in permeability of walls of collecting duct and distal convoluted tubule to water - causes more water to leave nephrons and be reabsorbed into the blood, so urine is more concentrated
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How does hypothalamus decrease water potential of blood
1. Wtaer potential of blood increases (too much water) 2. Detected by osmoreceptors in hypothalamus 3. Hypothalamus produces less ADH 4. Distal convoluted tubule and collecting duct walls become less permeable to water 5. Less water reabsorbed into blood and more is lost in urine (dilute urine) 6. Normal water potential of blood
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How does the hypothalamus increase water potential of blood
1. Water potential of blood decreases (not enough water) 2. Deeptected by osmoreceptors in hypothalamus 3. Hypothalamus produces more ADH - released into blood by posterior pituitary gland 4. Distal convoluted tubule and collecting duct walls become less permeable to water 5. More water reabsorbed into blood and less is lost in urine (concentrated urine) 6. Normal water potential of blood