ADH and aquaporin insertion in the collecting duct
Antidiuretic hormone (ADH) makes the collecting ducts (the last tubes of the nephron) insert aquaporins (water channels), so more water is reabsorbed when plasma osmolarity rises.
Remember
When plasma osmolarity rises, ADH inserts aquaporin channels into the collecting duct cells, which lets water return to the blood and dilutes the plasma.
Memory aid
the medulla is a salty sponge, and ADH is the tap that decides whether the collecting duct may use it.
Picture the salty medulla as a sponge that pulls on the water in the duct, with ADH deciding whether the duct wall lets the water through.
When water is lost as sweat and is not replaced, the plasma becomes more concentrated and plasma osmolarity rises. Osmoreceptors (sensors in the hypothalamus that detect how concentrated the blood is) respond by triggering release of ADH from the posterior pituitary gland (a small gland beneath the brain).
In the kidney, ADH acts through V2 receptors on collecting duct cells. The cells then insert aquaporins, which are protein pores that let water through, into the apical membrane on the side facing the urine.
The collecting duct passes down through the medulla (the inner kidney), and the tissue fluid around it is hyperosmotic (more concentrated than plasma). Because ADH has made the duct permeable to water, water moves out of the urine by osmosis and back into the blood. The kidney therefore conserves water, and the urine passed is small in volume and concentrated while the plasma is diluted.
When plasma osmolarity falls, ADH release is inhibited and the urine becomes dilute. The two responses form a feedback loop that stabilises osmolarity.
ADH conserves water but does not replace water already lost, so drinking is still needed. Thirst backs it up for larger changes: ADH release starts with a change of about 1% in plasma osmolarity, whereas thirst needs a larger change.
Key facts
- Trigger
- osmoreceptors in the hypothalamus detect a rise in plasma osmolarity, and ADH is released from the posterior pituitary gland.
- Site
- ADH acts on the collecting duct cells through V2 receptors.
- Mechanism
- ADH inserts aquaporins into the apical membrane of the collecting duct cells, which raises their water permeability.
- Result
- water is reabsorbed down the osmotic gradient into the medulla, giving a small volume of concentrated urine.
- Back-up
- thirst needs a larger change in plasma osmolarity than ADH release does, so ADH acts first and thirst takes over for larger changes.
- Limit
- ADH conserves water but does not replace water already lost, so drinking is still needed.
Exam traps
- The proximal tubule (the proximal convoluted tubule, the first coiled part of the nephron) has aquaporins that support water reabsorption, but ADH does not regulate them, so ADH inserts aquaporins into collecting duct cells instead.
- The loop of Henle (the hairpin-shaped part of the nephron) has an ascending limb, which carries fluid back up and is impermeable to water, so ADH does not vary the water permeability there: it varies that of the collecting ducts.
- ADH raises the permeability of the medullary part of the collecting duct to urea as well as to water, so a decrease in urea permeability is the opposite of its effect.
Read the full notes
Tested in 9 SimpleMed+ questions
Practice it in Urinary System, with the answer and a full explanation after every question.
Practice these questions