The shape of the lesson
By the end of the lesson, learners can
- Sensing water potential, releasing ADH: Choose dehydrated, normal and drunk a lot of water in turn.
- What the urine tells you: Compare the three states shown in the simulator with what happens to urine.
- Receptors: osmoreceptors in the hypothalamus.
- ADH made in the hypothalamus, released from the posterior pituitary.
- ADH → aquaporins inserted in the collecting duct luminal membrane.
- Water moves by osmosis; ADH only changes permeability.
One picture every idea returns to
Osmoregulation is the control of the water potential of the blood. Osmoreceptors in the hypothalamus detect it. When the water potential falls (after sweating, or eating salty food), they lose water by osmosis and shrink, stimulating neurosecretory cells; these made ADH (antidiuretic hormone) in the hypothalamus and it is released from their endings in the posterior pituitary gland into the blood. ADH binds to receptors on the cells of the collecting ducts, triggering vesicles containing aquaporins (water channel proteins) to fuse with the membrane facing the lumen. The duct wall becomes more permeable, more water moves by osmosis into the concentrated tissue fluid of the medulla and then the blood, and a small volume of concentrated urine is made. When the water potential rises, less ADH is released, aquaporins are taken back into vesicles and a large volume of dilute urine results. This is negative feedback.
Forty-five minutes, phase by phase
| Time | Phase | What happens in the room | Grouping |
|---|---|---|---|
| 0 to 5 min | Hook: predict | Open with the question in the title, One hormone, water channels on demand.. Sweat all afternoon and your urine turns dark and scant; drink a litre of water and it runs pale and plentiful. Put the figure on the board: it is the one picture every idea in the lesson returns to. | Whole class, then pairs |
| 5 to 17 min | Teach and check: Sensing water potential, releasing ADH | Choose dehydrated, normal and drunk a lot of water in turn. Project tab 5 of the lab (Homeostasis lab, ADH) and let a student drive it while the class predicts. | Whole class, then pairs |
| 17 to 30 min | Teach and check: What the urine tells you | Compare the three states shown in the simulator with what happens to urine. | Think-Pair-Share |
| 30 to 36 min | Check | The four Stage 1 questions from the student lesson, answered on mini whiteboards or by show of fingers. Re-teach the one most get wrong. | Individual, then whole class |
| 36 to 43 min | Plenary | The exam-style questions from Stage 2, one at a time: thirty seconds alone, then a random call. The feedback lines in the key give the examiner's wording. | Individual, random call |
| 43 to 45 min | Exit and homework | Set the worksheet below (6 questions, 18 marks). Learners self-assess against the objectives before they leave. | Individual |
Protect the parts that carry the learning
The sequence carries about fifty minutes of material, so the lab is driven by one student while the class predicts rather than explored freely. Times are a guide.
Protected: the check at 30 minutes. It is the only individual read on whether the key idea landed, and it is not cut.
Cut first if the build overruns: the last check in What the urine tells you, never the check or the plenary.
In a 60 minute block: run worksheet questions 1 to 3 in class as a Rally Coach set and model both the hardest worked example and its check live.
Think-Pair-Share
Pose the question, give thirty seconds of silent thinking, then a minute to compare with a partner before a few pairs share with the class. The silent minute is the part that cannot be cut.
The full structure, with its variations and the other twelve, is on the cooperative-learning page.
What to head off, and how
| Trap learners fall into | Teaching move that pre-empts it |
|---|---|
| ADH does not pump water. | It only changes the permeability of the collecting duct to water; the water moves passively by osmosis into the concentrated medulla. |
Osmoregulation and ADH: worksheet
6 questions, 18 marks. Written in the style of the papers; no past paper question is reproduced.
State what is meant by osmoregulation and name the receptors involved in mammals.
A runner loses a lot of water as sweat. Explain how the volume of urine produced is reduced.
Explain why the effect of ADH on the kidney is described as an example of negative feedback.
A person drinks 1 dm3 of water. Their urine flow rises from 1 cm3 min−1 to a peak of 9 cm3 min−1 after 45 minutes, then returns to 1 cm3 min−1 by 150 minutes. Explain these changes.
Suggest why alcohol, which reduces the release of ADH, can lead to dehydration.
Describe the roles of the hypothalamus, the posterior pituitary gland and the collecting ducts in osmoregulation.
Answer key and marking notes
- Osmoregulation is the control of the water potential of the blood / body fluids (keeping it within narrow limits).
- Osmoreceptors in the hypothalamus.
- The water potential of the blood falls, which is detected by osmoreceptors in the hypothalamus (they lose water and shrink).
- Neurosecretory cells release more ADH from the posterior pituitary gland into the blood.
- ADH binds to receptors on collecting duct cells; vesicles containing aquaporins fuse with the luminal membrane.
- The collecting duct becomes more permeable to water.
- More water moves by osmosis into the concentrated medulla / blood, so a small volume of concentrated urine is made.
- A fall in water potential leads to more ADH and more water reabsorption, which raises the water potential.
- As the water potential returns towards normal, osmoreceptors are stimulated less and less ADH is released.
- The response therefore reverses the original change and then switches itself off.
- The water is absorbed into the blood, raising its water potential; osmoreceptors are less stimulated and less ADH is released.
- Aquaporins are removed from collecting duct membranes, less water is reabsorbed and urine flow rises (a ninefold increase at the peak).
- As the excess water is excreted, blood water potential falls back to normal, ADH release increases again and urine flow returns to 1 cm3 min−1; the delay reflects the time for absorption and for ADH to be broken down.
- Less ADH means fewer aquaporins in the collecting duct membranes, so less water is reabsorbed.
- A large volume of dilute urine is produced, so the body loses more water than normal.
- Hypothalamus: contains osmoreceptors that detect the water potential of the blood; neurosecretory cells there make ADH.
- Posterior pituitary gland: stores ADH and releases it into the blood.
- Collecting ducts: the effector; ADH increases the number of aquaporins in their membranes, so more water is reabsorbed by osmosis.
8 multiple-choice questions on this lesson
From the topic question bank. Assign them in the app for a marked score in your gradebook, or run the topic as a class game.
Where are the receptors that detect changes in the water potential of the blood?
- Ain the hypothalamus
- Bin the posterior pituitary gland
- Cin the collecting ducts
- Din the loop of Henle
What is the direct effect of ADH on the cells lining the collecting duct?
- Avesicles containing aquaporins fuse with the membrane facing the lumen
- Bsodium ions are actively pumped out of the duct into the medulla
- Cthe cells become less permeable to water so more urine is produced
- Dglucose is cotransported out of the duct with sodium ions
A person eats a very salty meal and drinks nothing. Which set of changes follows?
- Ablood water potential falls, more ADH is released, less urine is produced
- Bblood water potential rises, less ADH is released, more urine is produced
- Cblood water potential falls, less ADH is released, more urine is produced
- Dblood water potential rises, more ADH is released, less urine is produced
Which describes how ADH reaches the kidney?
- Ait is made in the hypothalamus, released from the posterior pituitary and carried in the blood
- Bit is made in the posterior pituitary and carried along nerves to the kidney
- Cit is made in the anterior pituitary and released directly into the collecting duct
- Dit is made in the kidney cortex and diffuses into the medulla
Why does water move out of the collecting duct when aquaporins are present in its walls?
- Athe tissue fluid in the medulla has a lower water potential than the fluid in the duct
- BATP is used by the aquaporins to pump water out of the duct
- Cthe fluid in the duct has a lower water potential than the tissue fluid in the medulla
- Dthe hydrostatic pressure in the medulla is higher than in the duct
The graph shows how the concentration of ADH in the blood changes with the solute concentration of the plasma. Which conclusion is supported by the graph?
- Aabove about 280 units ADH rises steadily with solute concentration; below that, little ADH is released
- BADH rises in direct proportion to solute concentration over the whole range shown
- CADH is highest when the blood has the highest water potential
- DADH stops rising once the solute concentration reaches 300 units
In one form of diabetes insipidus, the collecting duct cells have faulty ADH receptors. Which combination of results is expected in an untreated person?
- Anormal or high ADH in the blood, large volumes of dilute urine
- Bvery low ADH in the blood, small volumes of concentrated urine
- Cvery low ADH in the blood, glucose present in the urine
- Dnormal ADH in the blood, small volumes of concentrated urine
Desert rodents have much longer loops of Henle, relative to kidney size, than mammals from wet habitats. How does this help them produce very concentrated urine when ADH is present?
- Aa longer loop builds up a lower water potential in the medulla, so more water leaves the collecting duct by osmosis
- Ba longer loop pumps more water out of the filtrate using ATP
- Ca longer loop increases the rate of ultrafiltration in the glomerulus
- Da longer loop produces more ADH, so more aquaporins are inserted
Quiz key
Osmoreceptors in the hypothalamus detect the water potential of the blood. The posterior pituitary gland stores and releases ADH but does not detect the change. The collecting ducts are the effectors that respond to ADH. The loop of Henle creates the concentrated medulla but has no receptor role.
ADH binds to receptors on collecting duct cells and causes vesicles carrying aquaporins (water channel proteins) to fuse with the luminal membrane, making it more permeable to water. Pumping sodium into the medulla is done mainly by the loop of Henle, not in response to ADH. Lower permeability is the effect of less ADH. Glucose cotransport happens in the proximal convoluted tubule.
Absorbed salt increases the solute concentration of the blood, lowering its water potential. Osmoreceptors are stimulated, more ADH is released and more water is reabsorbed in the collecting ducts, so a small volume of concentrated urine is produced. The other options either get the direction of water potential wrong or pair it with the wrong change in ADH and urine volume.
Neurosecretory cells in the hypothalamus make ADH; it passes down their axons to the posterior pituitary gland, where it is stored and released into the blood, which carries it to the kidney. The posterior pituitary does not make ADH, and no nerves run from it to the kidney. The anterior pituitary secretes other hormones. ADH is not made in the kidney.
The loop of Henle makes the tissue fluid of the medulla very concentrated, so its water potential is lower than that of the fluid in the duct; water moves down this gradient by osmosis through the aquaporins. Aquaporins are channels, not pumps, and use no ATP. If the duct fluid had the lower water potential, water would move in, not out. Hydrostatic pressure in the medulla is not what drives this movement.
Between 270 and 280 units the ADH concentration stays close to zero; above about 285 it rises steadily to about 5.5 units at 310. So ADH is released mainly when the solute concentration is raised. The line is not straight through the whole range, so it is not directly proportional. The highest solute concentration means the lowest water potential, not the highest. The line is still rising at 310, so it has not levelled off at 300.
Without working receptors, ADH cannot trigger the insertion of aquaporins, so little water is reabsorbed and a large volume of dilute urine is produced. The blood water potential then falls, which stimulates osmoreceptors, so ADH concentration stays normal or rises. Low ADH with concentrated urine is contradictory. Glucose in urine is a sign of diabetes mellitus, a different condition. Concentrated urine would require the collecting duct to respond to ADH.
The loop of Henle builds up a high solute concentration in the medulla; a longer loop makes the medulla even more concentrated, so its water potential is very low. When ADH makes the collecting duct permeable, more water moves out by osmosis and the urine becomes very concentrated. Water is never pumped; it moves by osmosis. The loop does not affect filtration in the glomerulus, and ADH is made in the hypothalamus, not the kidney.
What to project
The student lesson embeds these tabs. Open them full screen on the projector; every slider has a drag handle on the stage.
Slides for this lesson
A projectable deck for every pack is on the way. Until then, present the student lesson full screen: its sections, figure and lab tabs follow the same order as the plan above.