By responding to changes in their environment, organisms increase their chance of

survival

1. Stimulus - detectable change in the

internal/external environment of an organism
that leads to a response
2. Receptor – detects stimulus, specific to one
type of stimulus
3. Coordinator – formulates a suitable response
to a stimulus e.g. nervous system / hormonal
system
4. Effector – produces response to a stimulus e.g.
muscles / glands
5. Response 


The protective effect of a simple reflex, exemplified by a three neurone simple reflex

- Reflex arc: stimulus→ receptor → sensory neurone → coordinator – CNS / relay neurone →
motor neurone → effector → response
- Importance:
- Rapid (short pathway) because only 3 neurones and few synapses (synaptic transmission
is slow)
- Autonomic because doesn’t involve passage to brain – doesn’t have to be learnt
- Protect from harmful stimuli e.g. escape from predator / prevents damage to body
tissues

Taxes and kineses as simple responses that can maintain a mobile organism in a
favourable environment

- Taxes – Directional responses by simple mobile organisms who move towards a favourable
stimulus (positive taxis) or away from an unfavourable one (negative taxis)
- Example: Woodlice show a tactic response to light. Move away from light → keeps
concealed under stones during day away from predators, and in damp conditions which
reduces water loss → improves chances of survival
 - Kineses – Non-directional responses by simple mobile organisms who change the speed of
movement or the rate of direction change, in response to a non-directional stimulus
- Example: Woodlice show a kinetic response to humidity. Move faster/change direction
more often when air drier → increases chances of moving to an area of higher humidity
where lose less water → improve chances of survival

Tropisms and growth factors in (flowering) plants

- Tropism – growth of a part of a plant in response to a directional stimulus.

- Positive tropism – growth towards stimulus
- Negative response – growth away from stimulus

- Plant responses to external stimuli involve growth factors / hormone-like growth substances
- Growth factors move from growing regions e.g. shoot tips / leaves where they are produced, to
other tissues, where they regulate growth in response to directional stimuli e.g. Auxins (such as
IAA)

Gravitropism and phototropism explained by indoleacetic acid (IAA):

- In roots, IAA inhibits cell elongation; whereas in shoots, IAA promotes cell elongation

How IAA results in phototropism in shoots:

- Cells in tip of shoot produce IAA → transported down shoot (evenly initially) 

- IAA conc increases on shaded side
- Promotes cell elongation
- Shoot bends towards light 


How IAA results in gravitropism in roots:

- Cells in tip of shoot produce IAA → transported down shoot (evenly initially)
- IAA conc increases on lower side of root
- Inhibits cell elongation
- Root curves downwards towards gravity

The Pacinian corpuscle

- Generating a generator potential

- Mechanical stimulus e.g. pressure
deforms lamellae and stretch-
mediated sodium ion channel
- Sodium ion channels open and sodium ions diffuse into sensory neurone
- Greater pressure causes more channels to open and more sodium ions to enter
- Causes depolarisation, leading to a generator potential
- *If generator potential reaches threshold it triggers an action potential
- What does the Pacinian corpuscle illustrate?
- Receptors respond only to specific stimuli – 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
The human retina – differences in sensitivity to light, colour and visual acuity are
explained by differences in the optical pigments of rods and cones and the they make
in the optic nerve

Summary of the differences between cones and

rods
Rods Cones
More at periphery of Concentrated at fovea
retina Fewer at periphery of
Absent in fovea retina
One type of rod 3 types of cones
containing one pigment containing different
optical pigments
Rods connected in One cone joins one
groups to one bipolar neurone
cell / ganglion cell /
neurone
Very sensitive to light Less sensitive to light
(see in dim light) (require bright light)
Low visual acuity High visual acuity

Black & white Colour (trichromatic)

(monochromatic) vision
vision

Describe and explain differences in sensitivity to light

- Rods are more sensitive to light

- Rods connected in groups to one bipolar cell / ganglion cell / neurone (retinal
convergence)
- Spatial summation
- Stimulation of each individual-cell alone is sub-threshold / insufficient but cells connected
in groups means threshold more likely met/ exceeded to generate action potential
- Cones are less sensitive to light / need higher intensity light
- One cone joins to one neurone
- No spatial summation

Describe and explain differences in visual acuity

- Cones give higher visual acuity

- One cone joins to one neurone
- If 2 adjacent cone cells are stimulated, brain receives 2 separate impulses (information)
→ can distinguish between 2 separate sources of light
- Rods give lower visual acuity
- Rods connected in groups to one bipolar cell / ganglion cell / neurone (retinal
convergence)
- Spatial summation
- Many neurones only generate one impulse / action potential, regardless of how many
neurones stimulated → can’t distinguish between separate sources of light
Describe and explain differences in sensitivity to colour

- Cones allow colour vision

- 3 types of cones
- With different optical pigments that absorb different wavelengths / red / green / blue
- Stimulation of different combinations / proportions of cones gives a range of colour
perception
- Rods allow monochromatic vision
- One type of cone / pigment

Example exam question

Figure 1 shows where two types of light receptor cells, P and S, are found in the retina of the human
eye.

(a) A person cannot see an object if its image falls on R. Explain why. (1 mark)

✓ No receptors at R

(b) At night, a man saw a faint star at the edge of his vision. When he moved his eyes to look
straight at the star, he could no longer see it.
Use the information from figure 1 to explain

(i) Why he could see the star at the edge of his vision. (2 marks)

✓ Image falls on rods / S = rods

✓ Summation
✓ Faint light from star will stimulate rods

(ii) Why he could not see the star when he looked straight at it. (2 marks)

✓ Image falls on fovea

✓ Cones present at fovea / P = cones
✓ One cone per neurone
✓ Cones / P need high light intensity to stimulate them / faint light will not stimulate them
Myogenic stimulation of the heart and transmission of a subsequent wave of electrical
activity. The roles of the SAN, AVN and Purkyne tissue in the bundle of His

- Cardiac muscle is myogenic i.e. it can contract/relax without receiving electrical impulses from
nerves
- Sinoatrial node (SAN) acts as a pacemaker and sends out regular waves of electrical across both
atria
- Causing right/left atria to contract simultaneously
- (A layer of non-conductive tissue prevents wave crossing directly to ventricles)
- Waves of electrical activity reaches the atrioventricular node (AVN) which delays impulse,
allowing atria to fully contract and empty
- AVN passes wave of electrical activity to bundle of His which conducts wave between ventricles
to the apex of the heart, where the bundle branches into smaller fibres of Purkyne tissue
- Ventricles contract simultaneously, from the bottom up

The roles and locations of chemoreceptors and pressure receptors and the roles of the
autonomic nervous system and effectors in controlling heart rate

- Baroreceptors and chemoreceptors located in aorta and carotid arteries

- Baroreceptors stimulated by high/low blood pressure
- Low BP – more frequent impulses to medulla / cardiovascular control centre – more
frequent impulses sent to SAN along sympathetic neurones – more frequent impulses
sent from SAN – cardiac muscle contracts more frequently so heart rate increases
- High BP – more frequent impulses to medulla / cardiovascular control centre – more
frequent impulses sent to SAN along parasympathetic neurones – less frequent impulses
sent from SAN – cardiac muscle contracts less frequently so heart rate decreases
- Chemoreceptors stimulated by blood pH / CO2 conc. / O2 conc. (related to exercise)
- High blood CO2 conc. / low pH – more frequent impulses to medulla / cardiovascular
control centre – more frequent impulses sent to SAN along sympathetic neurones –
more frequent impulses sent from SAN – cardiac muscle contracts more frequently so
heart rate increases
- Low blood CO2 conc. / high pH – more frequent impulses to medulla / cardiovascular
control centre – more frequent impulses sent to SAN along parasympathetic neurones –
less frequent impulses sent from SAN – cardiac muscle contracts less frequently so heart
rate decreases

Example exam question

Increased intensity of exercise leads to an increased heart rate. Explain why. (3 marks)

✓ (Oxygen/carbon dioxide) detected by chemoreceptors / (pressure) detected by baroreceptors

✓ Medulla / cardiac centre involved
✓ More impulses to SAN / along sympathetic nerve
Structure of a myelinated motor neurone

The establishment of a resting potential

- Sodium-potassium ion pump actively transports:

- 3 sodium ions out of axon
- 2 potassium ions into axon
- Electrochemical (concentration)
gradient created e.g. higher conc. of
potassium ions inside axon than outside,
higher conc. of sodium ions outside axon
than outside
- Membrane more permeable to
potassium ions (open K+ channels) than
sodium ions (closed Na+ channels)
- Potassium ions move out of axon by
facilitated diffusion Inside of axon
negatively charged relative to outside;
axon is polarised = resting potential
Changes in membrane permeability lead to depolarisation and the generation of an
action potential. The all-or-nothing principle

- Stimulus
- Membrane more permeable to sodium ions as sodium ion channels open
- Sodium diffuse into neurone down electrochemical gradient
- Depolarisation
- P.d. reaches threshold, action potential generated
- Because more voltage-gated sodium ion channels open and sodium diffuse rapidly
- Repolarisation
- Sodium ion channels close (membrane less permeable to sodium ions) whilst (voltage-
gated) potassium ion channels open so potassium ions diffuse out of neurone
- Hyperpolarisation
- Potassium ion channels slow to close so there’s a slight overshoot – too many potassium
ions diffuse out of neurone
- Resting potential restored
- By sodium-potassium pump
- Note: bigger stimulus will cause more frequent action potentials but they will all be the same
size
Example exam question

During an action potential. The permeability of the cell-surface membrane of an axon changes. The
graph shows changes in permeability of the membrane to sodium ions (Na+) and to potassium ions
(K+) during a single action potential.

(a) Explain the shape of the curve for sodium ions between 0.5ms and 0.7ms. (3 marks)

✓ (Ion) channel proteins open

✓ Sodium in
✓ Changes membrane potential / makes inside of axon less negative / depolarisation / reaches
threshold
✓ More channels open / positive feedback

(b) During an action potential, the membrane potential rises to +40mV and then falls. Use
information from the graph to explain the fall in membrane potential. (3 marks)

✓ Potassium channels open

✓ Potassium out
✓ Sodium channels close

The nature and importance of the refractory period

- Refractory period is the time to restore axon to resting potential / no further action potential
can be generated
- Importance:
- Produces discrete and discontinuous impulses (action potentials don’t overlap)
- Limits frequency of impulse transmission at a certain intensity (limits strength of stimulus
that can be detected); higher intensity stimulus causes higher frequency of action
potentials but only up to certain intensity
- Unidirectional action potential – can’t be propagated in a region that is refractory

Factors affecting the speed of conductance

- Myelination
- Depolarisation at Nodes of Ranvier only → saltatory conduction (impulse jumps from
node to node)
- Impulse doesn’t travel whole axon / no need to depolarise along whole length of axon
unlike non-myelinated neurone
 - Axon diameter
- Bigger diameter means less leakage of ions / less resistance to flow of ions
- Temperature
- Increases rate of movement of ions Na+ and K+ as more kinetic energy (active transport /
diffusion)
- Higher rate of respiration (enzyme activity faster) so ATP produced faster and energy
released faster → active transport faster
- But proteins could denature at a certain temperature

The passage of an action potential along non-myelinated and myelinated axons,

resulting in nerve impulses

- Non-myelinated axon
- Action potential passes as a wave of depolarisation
- Influx of sodium ions in one region increases permeability of adjoining region to sodium
ions by causing voltage-gated sodium ion channels to open so adjoining region
depolarises
- Myelinated axon
- Depolarisation of axon at nodes of Ranvier only
- Resulting in saltatory conduction
- So there is no need for depolarisation along whole length of axon

Example exam question

Multiple sclerosis (MS) is a disease that involved damage to the myelin sheaths of neurones. Movement
in MS sufferers may be jerky or slow.

Damage to the myelin sheaths of neurones can lead to problems controlling the contraction of
muscles. Suggest one reason why. (2 marks)

✓ Action potentials travel more slowly / don’t travel / no salutatory movement of potentials
✓ So delay in muscle contraction / muscles don’t contract / muscles contract slower
OR
✓ Action potentials / depolarisation ‘leaks’ to adjacent neurones
✓ So wrong muscle (fibres) contract

Structure of a synapse and of a neuromuscular junction

Synapse
Neuromuscular junction

Transmission across a cholinergic synapse

1. Action potential arrives causing calcium ion channels to open → calcium ions diffuse into pre-
synaptic neurone
2. Causing vesicles containing neurotransmitter / acetylcholine (which is made only in the
presynaptic neurone) to fuse to pre-synaptic membrane → release acetylcholine into synaptic
cleft (exocytosis)
3. Neurotransmitters diffuse across synaptic cleft → bind to specific neurotransmitter receptors
found only on post-synaptic membrane
4. Sodium ion channels open → sodium ions diffuse into post-synaptic knob → depolarisation
initiates action potential (excitatory synapse)
5. Neurotransmitter removed from cleft so response doesn’t keep happening e.g. broken down by
an enzyme called acetylcholinesterase (AChE) and the products are reabsorbed by the
presynaptic neurone

Comparison of transmission across cholinergic synapses and neuromuscular junctions

- Cholinergic synapse - neurone to neurone WHEREAS neuromuscular - neurone to muscle

- Neuromuscular junction: ACh is always excitatory and never inhibitory, so always triggers
generator/action potential
- Neuromuscular junction: Post-synaptic membrane has more receptors than other synapses
- Neuromuscular junction: Lots of folds on post-synaptic membrane which form clefts to store
enzyme (Acetylcholinerase / AChE) to break down neurotransmitter (Acetylcholine / Ach)

Why synapses result in unidirectional nerve impulses

- Neurotransmitter only made in / released from pre-synaptic neurone

- (Neuro)receptors only on post-synaptic membrane

Summation – temporal and spatial

- Summation: Addition of a number of impulses converging on a single post-synaptic neurone

- Spatial summation
- Many pre-synaptic neurones share the same synaptic cleft / post-synaptic neurone
- Collectively release sufficient neurotransmitter to reach threshold to trigger an action
potential
 - Temporal summation
- One pre-synaptic neurone releases neurotransmitter many times over a short period / in
rapid succession
- Sufficient neurotransmitter to reach threshold to trigger an action potential
- Important because low frequency action potentials often release insufficient amounts of
neurotransmitter to exceed threshold in post-synaptic neurone → summation allows an action
potential to be generated by the build-up of neurotransmitter

Inhibition by inhibitory synapses

- Inhibitory neurotransmitters hyperpolarise the

postsynaptic membrane
- K+ channels open – K+ diffuse out
- Cl- channels open – Cl- diffuse in
- Inhibits formation of action potential /
transmission of nerve impulses by post-synaptic
membranes
- Can’t be depolarised
- Reduces the effect of sodium ions entering
so much less likely to reach threshold
- Example: Acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in the heart
- Note: By having both excitatory and inhibitory neurones forming synapses with the same post-
synaptic membrane, this gives control of whether post-synaptic membrane ‘fires’ or not,
therefore ‘firing’ is not inevitable and stimulation can be overridden

Using information provided, predict and explain the effects of specific drugs on a
synapse

Way 1: Stimulate nervous system à more action potentials e.g. mimic neurotransmitter / stimulate release
of more neurotransmitter / inhibit enzyme that breaks down neurotransmitter

Example: GABA is a neurotransmitter produced by neurones in the brain and spinal cord. It binds to
post-synaptic membranes and inhibits the production of nerve impulses. Epilepsy may result when
there is increased neuronal activity in the brain. One form of epilepsy is due to insufficient GABA. GABA
is broken down on the post-synaptic membrane by transaminase. Vigabitrin is a new drug being used to
treat this form of epilepsy. It has a similar molecular structure to GABA.

✓ Binds to GABA receptors à Inhibits neuronal activity / chloride ions enter neurone
✓ OR inhibits enzyme which breaks down GABA à more GABA available

Example: Black mamba’s toxin prevents breathing. Inhibits Acetylcholinesterase at neuromuscular

junctions.

✓ ACh not broken down / stays bound to receptor

✓ Na+ ions continue to enter / depolarisation continues / Na+ channels kept open / action
potentials or impulses fired continuously
✓ Intercostal muscles stay contracted / can’t relax

Example: This synapse uses a neurotransmitter called dopamine. Cocaine is a similar shape to
dopamine. Cocaine binds to the dopamine transporter (transports dopamine back to pre-synaptic
knob). It is released in parts of the brain where pleasure is perceived and can result in feelings of
pleasure.
 ✓ Dopamine and cocaine have similar shapes / so it can fit into the transporter
✓ Blocks transport of dopamine out of synaptic cleft into pre-synaptic knob
✓ Dopamine concentration rises / remains and continues to bind to receptor
✓ Continued firing of impulses in post-synaptic neurone

Way 2: Inhibit nervous system à fewer action potentials e.g. inhibit release of neurotransmitter / block
receptors

Example: Pancuronium binds to acetylcholine receptors on muscle fibres, causing muscle paralysis.

✓ Pancuronium is a similar shape to acetylcholine so is complementary to / fits in receptor and can

bind to
✓ Not broken down / removed from receptor by AChE so blocks receptor site / prevents ACh from
binding
✓ Na+ channels on membrane don’t open so no action potential, and no influx of Ca2+ ions to
start contraction, so prevents unblocking of binding sites on actin

Example: Cannabinoids prevent muscle contraction. They are hydrophobic and easily pass into
neurones. Cannabinoid receptors are found in pre-synaptic membrane of neuromuscular junctions.
When a cannabinoid binds to its receptor, it closes calcium ion channels.

✓ Prevents influx of calcium ions into presynaptic membrane

✓ Synaptic vesicles don’t fuse with membrane / release ACh so ACh doesn’t diffuse across synapse
/ bind to receptors on post-synaptic membrane
✓ No action potential / depolarisation of post-synaptic membrane / sodium ion channels don’t
open / prevents influx of sodium ions

Example: Enkephalins are neurotransmitters released by the brain and spinal cord in response to
harmful stimuli. They’re similar in shape to acetylcholine. They act as painkillers by inhibiting synaptic
transmission.

✓ Bind to receptors on post-synaptic membrane as complementary to receptors

✓ Acetylcholine can’t bind so reduces / stops depolarisation

Muscles act as antagonistic pairs against an incompressible skeleton

- Muscles work in antagonistic pairs

- One muscle contracts (agonist) → pulls on bone / produces force
- One muscle relaxes (antagonist)
- Examples: biceps and triceps in the arm
- Attached to bones by tendons
- Ligaments attached from one bone to the other
- Skeletal muscle is incompressible so muscle can transmit force to bone
- Advantages of skeletal muscles being arranged in antagonistic pairs
- Muscles can only contract / pull
- 2nd muscle required to reverse the movement caused by 1 st
- Help maintain posture → contraction of both muscles
Gross and microscopic structure of skeletal muscle

- Muscle made up of bundles of muscle fibres (muscle cell) packaged together

- Muscle cells contain
- Cell membrane =
sarcolemma
- Cytoplasm =
sarcoplasm
- Myofibrils made
up of two
proteins, actin
and myosin
- Shared nuclei
- Lots of
endoplasmic
reticulum

Ultrastructure of a myofibril

- Myofibril made up of many sarcomeres which are made up of partly overlapping myosin and
actin filaments (proteins)

- A sarcomere consists of
- Ends – Z-line
- Middle – M-line
- H zone – around M line which contains only myosin
- Myosin filaments are thicker than thinner actin filaments
- This causes a banding pattern to be seen (in a relaxed myofibril) under an electron microscope:
- I-bands → light bands containing only thick actin filaments
- A-bands → dark bands containing thick myosin filaments and some overlapping actin

Muscle contraction

- Myosin heads slide actin past/along myosin causing the sarcomere to contract
- Simultaneous contraction of lots of sarcomeres causes myofibrils and muscle fibres to contract
- When sarcomeres contract (shorten)…
- H zones shorter
- I band shorter
- A band same
- Z lines closer
The roles of actin, myosin, calcium ions and ATP in myofibril contraction

The process is as follows, but use this key so you can pick out the key points to answer questions about
the roles of actin, myosin, calcium ions and ATP in contraction
Example exam question

The diagram in figure 1 shows the arrangement of actin and myosin in a sarcomere.

One form of muscle disease is caused by a mutated allele of a gene. This leads to production of myosin
molecules that are unable to bind to other myosin molecules.

If myosin molecules are unable to bind to other myosin molecules, this prevents muscle contraction.

Use figure 1 and your knowledge of how muscles contract to suggest why. (3 marks)

✓ Can’t form myosin / thick filaments

✓ Can’t pull / can’t move actin / slide actin past / (myosin) have to be joined / fixed to full actin
✓ Myosin moves/ if attached doesn’t move
✓ Can’t move actin towards each other / can’t shorten sarcomere / can’t pull Z lines together

Structure, location and general properties of slow and fast skeletal muscle fibres

Slow twitch

- Specialised for slow, sustained contractions (endurance)

- Endurance activities e.g. maintaining posture, long distance running
- Located in muscles that give posture and in leg muscles of long distance runners, for example
- Aerobic respiration produces ATP (oxidative phosphorylation) to release energy slowly
- High levels of myoglobin (red coloured protein that stores oxygen) makes them a reddish colour
→ store large amount of oxygen in muscle for aerobic respiration
- Many mitochondria (site of aerobic respiration) → high rate of aerobic respiration
- Many capillaries → short diffusion pathway / large surface area → supply high conc. of oxygen /
glucose (little / no glycogen / myoglobin) for aerobic respiration and to prevent build-up of lactic
acid causing muscle fatigue 

Fast twitch

- Specialised for producing rapid, intense contractions of short duration

- Short bursts of speed and power e.g. sprinting
- Located in the legs of sprinters, for example
- Anaerobic respiration produces ATP to release energy quickly
- Low levels of myoglobin makes them a whitish colour → anaerobic respiration doesn’t need
oxygen
- Lots of glycogen → hydrolysed to lots of glucose → used during glycolysis (anaerobic
respiration) which is inefficient, yielding only 2 ATP per glucose molecule 

- Higher conc. of enzymes involved in anaerobic respiration (in cytoplasm) → high rate of
anaerobic respiration
- Store phosphocreatine which rapidly generates ATP from ADP by providing phosphate 

- Muscles can get fatigued quickly because of high amounts of lactate

Role of phosphocreatine in muscle contraction

- Phosphocreatine stored inside cells

- Rapidly makes ATP by phosphorylating ADP (adding phosphate group from PCr)
- PCr runs out after a few seconds so it’s used in short bursts of vigorous exercise
- Anaerobic and alactic
Importance of maintaining stable core temp and blood pH
a) Stable core temp
- Enzymes work at an optimum temp
- Too low → not enough Ek → fewer successful collisions / enzyme-substrate complexes
- Too high → enzymes denature as H bonds in tertiary structure break → active site changed
shape and no longer complementary to substrate → fewer successful collisions / enzyme-
substrate complexes 


b) Stable blood pH 

- Enzymes work at an optimum pH
- Too low / high → enzymes denature as ionic bonds in tertiary structure break → active site to
change shape so no longer complementary to substrate → fewer successful collisions and
enzyme-substrate complexes 


Importance of maintaining a stable blood glucose concentration 


- Too low (hypoglycaemia)

- Not enough glucose for respiration (particularly brain + nervous system) so less ATP
produced
- Active transport etc. can’t happen
- Too high (hyperglycaemia)
- Blood has low water potential (as increased solute)
- Water lost from tissue to blood via osmosis
- Kidneys can’t absorb all glucose → more water lost in urine causing dehydration

Negative vs. positive feedback

- Negative feedback
- Receptors detect levels too low / high à
effectors respond to counteract change
- Restores levels to normal / original
- Example: regulation of body temperature
- Positive feedback
- Amplifies change from normal level
- Advantage – rapidly activate something
e.g. blood clot
- Not involved in homeostasis
- Homeostasis involves multiple negative
feedback mechanisms
- More control over changes in internal environment
- Controls departures in different directions from the original state / actively increase or
decrease a level to normal
- Faster response
Factors that influence blood
glucose concentration

- Eating food containing

carbohydrates → glucose
absorbed from intestine to
blood
- Exercise → increase rate of
respiration of glucose

Action of insulin

- Secreted by beta cells in islets of Langerhans in pancreas when blood glucose concentration is
too high
- Insulin binds to specific receptors on cell surface membranes of liver / muscle cells (target cells)
- Increases permeability of muscle cell membrane to glucose → by increasing number of
channel proteins
(GLUT4) in cell surface membrane → cells uptake more glucose from
blood by facilitated diffusion
- Activation of enzymes in liver / muscle cells that convert glucose to glycogen
(glycogenesis) → store glycogen in cytoplasm
- Rate of respiration of glucose also increases 

- DECREASES blood glucose concentration 


Action of glucagon

- Secreted by alpha cells in islets of Langerhans in pancreas when blood glucose concentration is
too low
- Binds to specific receptors on cell surface membranes of liver cells (target cells)

- Activates enzymes involved in the conversion of glycogen to glucose (glycogenolysis)
- Activates enzymes involved in the conversion of glycerol / amino acids to glucose
(gluconeogenesis)
- Rate of respiration of glucose also decreases
- INCREASES blood glucose concentration

Role of adrenaline

- Secreted by adrenal glands (above kidneys) when blood glucose concentration is low / stressed /
exercising
- Binds to specific receptors on cell surface membranes of liver cells (target cells)
- Activates enzymes involved in the conversion of glycogen to glucose (glycogenolysis)
- Inhibits glycogenesis
- Activates secretion of glucagon

- INCREASES blood glucose concentration (more glucose for respiration) 

Secondary messenger model 


- Adrenaline and glucagon demonstrate

this because they cause glycogenolysis
to occur inside cell even though they
bind to receptors on the outside of the
cell
1. Adrenaline / glucagon bind to specific
complementary receptors on cell
membrane
2. Activate adenylate cyclase
3. Converts ATP to cyclic AMP
(secondary messenger)
4. cAMP activates protein kinase A
(enzyme)
5. Protein kinase A activates a cascade to
break down glycogen to glucose
(glycogenolysis)

Diabetes

Diabetes is where blood glucose concentration can’t be controlled properly. Blood glucose
concentration peaks higher and takes longer to decrease / remains high (after meal)

Type I
Cause Gene mutation → Autoimmune
response on B cells of islets on
Langerhans →Body can’t produce
insulin
Control: - Injections of insulin (not by
insulin mouth as protein is digested)
- Dose of insulin matched to
glucose intake / use biosensors
Control: diet - Eating regularly, control
manipulation carbohydrate intake e.g. carbs
which are broken down /
absorbed slower
- Avoid sudden rise in glucose
Type II
Poor diet / lack of exercise / obesity→
Glycoprotein / receptor loses responsiveness
to insulin (faulty) → cells less responsive to
insulin / don’t take up enough glucose
- Use of drugs which target insulin
receptors / use of insulin
- More glucose uptake by cells / tissues
- Reduced sugar intake (carbs) in diet /
eat food with low glycaemic index
→ Less sugar absorbed into blood
- Reduced fat intake

→ Less fat converted to glucose
- More (regular) exercise
→ Uses glucose / fats by increasing
respiration
- Lose weight
→ Increased sensitivity of cells to
insulin / increased uptake of glucose by
cells 


Evaluate the positions of health advisers and the food industry in relation to the
increased incidence of type II diabetes
Example exam question

Figure 11 shows how the blood glucose concentration of a healthy, non-diabetic person varied over 24
hours.

a) The person ate 3 carbohydrate-rich meals at the times shown in figure 11

i) Write the letter X on figure 11 to show one time when the insulin concentration would be
highest (1 mark)
✓ ‘X’ on either side or both of the glucose peaks at 08:30 / 16:30
ii) Explain why you chose this time (1 mark)
✓ Insulin lowers blood glucose / stimulates uptake of glucose by cells / by liver / by muscles
OR
✓ High blood glucose stimulates insulin secretion
iii) Figure 11 shows blood glucose concentration in a healthy, non-diabetic person. Describe two
ways in which a similar graph, drawn for a diabetic person, would differ from this. (2 marks)
✓ Higher glucose concentrations in diabetic
✓ Takes longer time to decrease / remains high (after each meal)
Example exam question

Type 1 diabetes inject insulin.

Different forms of modified human insulin are available for diabetics to use.

Scientists investigated the activity in the blood of two modified forms of human insulin, N and G. One
group of diabetics injected themselves with insulin-N. The second group injected themselves with
insulin-G. The scientists then measured the activity of the insulin in blood samples taken from each
group at hourly intervals over the next 24 hours.

Their results are shown in figure 9.

Suggest how each of these two types of insulin might be used to manage a patient’s diabetes. (4
marks)

✓ N – has high activity / acts quickly

✓ N – will lead to greater/faster lowering of blood glucose (than G)
✓ N – (relatively) short-lived effect
✓ N – may need >1 injection per day
✓ N – useful around meal times
✓ G – fairly constant level of insulin (activity)
Osmoregulation

- Osmoregulation is the control of water and salt levels in the body

- Controlled by hormones e.g. antidiuretic hormone (ADH) which affect the distal convoluted
tubule and collecting duct

Roles of hypothalamus, posterior pituitary and antidiuretic hormone (ADH) in

osmoregulation 


How the body responds to a decrease in water potential... 


1. Detected by osmoreceptors in hypothalamus

2. Hypothalamus produces more ADH → posterior pituitary gland secretes more ADH into blood 

3. ADH travels in blood to kidney and attaches to receptors on collecting duct / DTC of kidney 

4. ADH increases permeability of cells/walls of the DTC / collecting duct (more aquaporins fuse with
cell membrane) to water → more water absorbed from/leaves DCT/collecting duct by osmosis
5. (Less water lost in urine so) smaller volume of urine, more concentrated 


Note: This only stops water potential of blood becoming lower. Impulses also sent to brain to
encourage drinking

How the body responds to an increase in water potential...

1. Detected by osmoreceptors in hypothalamus

2. Hypothalamus produces less ADH → posterior pituitary gland secretes less ADH into blood 

3. Less ADH travels in blood to kidney and attaches to receptors of collecting duct / DTC of kidney
4. ADH decreases permeability of cells/walls of the DTC / collecting duct to water and urea to water
 → less water absorbed from/leaves DCT/collecting duct by osmosis
5. (More water lost in urine so) larger volume of urine, less concentrated 


Note: As the water potential of blood falls, negative feedback stops it becoming too low

Role of nephron in osmoregulation:

Formation of glomerular filtrate → reabsorption of glucose and water by the proximal convoluted
tubule → maintenance of a gradient of sodium ions in the medulla by the loop of Henle → reabsorption
of water by the distal convoluted tubule and collecting duct

a) Formation of glomerular filtrate

- Diameter of efferent arteriole

smaller than afferent arteriole
- Build-up of hydrostatic pressure
in glomerulus
- Water, glucose, mineral ions
squeezed out of capillary /

glomerulus into the Bowman’s
capsule to form
glomerular
filtrate

- Through pores in capillary
endothelium, basement
membrane and
podocytes (act as filter)
- Large proteins / blood cells
aren’t pushed out as too large 


b) Reabsorption of glucose and water by the proximal convoluted tubule

1. Sodium ions actively transported out

of epithelial cell to capillary
- Lowers concentration of Na+ in
epithelial cell
2. Na+ moves via facilitated diffusion
from PCT into epithelial cell down
concentration gradient
- Co-transporting glucose / amino
acids / Cl-
- Increases concentration of
glucose etc. in epithelial cell 

3. Glucose / amino acids / Cl- move into
capillary via facilitated diffusion down
concentration gradient (reabsorbed)
- Lowers water potential in
capillary
4. Water moves via osmosis down water
potential gradient into capillary
(reabsorbed)


 c) Maintaining a gradient of sodium ions in the medulla by the loop of Henle

1. Loop of Henle acts as a counter current

multiplier → maintains water potential
gradient → water leaves collecting duct
/DCT by osmosis 

2. Na+ actively transported out of
ascending limb and ascending limb is
impermeable to water so water remains

- Increases conc of Na+ in medulla →
lowers water potential 

3. Water moves out of descending limbs /
collecting duct by osmosis into medulla 

- Water reabsorbed by capillaries 

- Filtrate more concentrated as move
down the ‘hairpin’ 

4. Na+ diffuse into descending limb 

- Recycles Na+ in loop of Henle
- Reduces water potential further 


d) Reabsorption of water by the distal convoluted tubule and collecting ducts

- Water moves out of the DCT and collecting duct by osmosis down a water potential
gradient 

- Controlled by ADH which changes their permeability 


Example exam question:

The whale is a large mammal that lives in the sea.

Whales take in sea water with their food. They have adaptations that prevent them from dehydrating
when they take in sea water. Humans do not have such adaptations. If humans drink sea water they
become dehydrated.

Scientists measure the volume of urine produced by whales and by humans when they take in sea
water. They also measured the chloride ion content of the urine produced by humans and by whales.
Sea water has a chloride concentration of 535 mmol dm-3.

The table shows the results.

a) Use the data in the table to explain

i) Why a human who drinks sea water becomes dehydrated (1 mark)
✓ Greater urine production than water intake
ii) How a whale is adapted to be able to drink sea water (1 mark)
✓ Low volume of concentrated urine
b) Long loops of Henle enable the whale to produce very concentrated urine. Explain how. (3
marks)
✓ High concentration of sodium (ions)/chloride (ions)/salts surrounding the loop
✓ Active removal of ions from ascending limb which is impermeable to water / due to
counter-current multiplier
✓ (With long loops there will be a) greater gradient/difference in water potential between
collecting duct and medulla
✓ Greater uptake of water from collecting duct