Physiology 3120 Lecture Notes - Lecture 7: Aquaporin 2, Osmosis, Diuretic
9 May 2018
School
Department
Course
Professor
Physiology 3120
Dr. Woods
Lecture 7
Plasma Osmolarity and ADH Release
- ADH has a very short plasma life (couple of minutes) so in order for it to continue doing its job
reabsorbing water, you need constant ADH being released into the blood
- The higher the concentration of ADH, the more water will be reabsorbed by the collecting duct
- Plasma osmolarity can change a lot from day to day
- If you decide you are going to drink 1L of water, you will change your plasma osmolarity by 7-
8mOsm depending on your mass
- So if you’re an avg 70kg individual, its about a 7-8mOsm change
- The change in osmolarity is very detectable – your neuroendocrine cells will start responding by
releasing more or less ADH at 1-2mOsm differences
- So it’s a very small, sensible, detectable change
- Osmolarity, in the normal range, is the most important factor – most sensitive input that these
hypothalamic neurons will receive
- Recall: osmolarity is detected by osmoreceptors (neurons that are found with and around the
hypothalamus)
- The osmoreceptors are found near the 3rd ventricle in your brain, near the hypothalamus
- There are fenestrated capillaries in that ventricle that allow for quick changes in interstitial fluid
composition
- So although the blood is not in your brain, we have compartments that can detect osmolarity
changes very quickly
- If the osmolarity was to increase (think about the ratio of solutes to water), the osmoreceptors
will respond by changing the activity of the neuroendocrine cells
- Higher plasma osmolarity will cause shriveling of the actual cell bodies of the osmoreceptors
- This leads to more AP
- So a physically decrease in cell volume of the osmoreceptors will cause them to send more AP
- Those neurons will synapse on the hypothalamic neurons that make ADH
- But remember that ADH is stored in the posterior pituitary so it is then released from there
o So the ADH is released from the posterior pituitary but the cell bodies of those neurons
are located in the hypothalamus
- Once we have ADH going through the blood that travels through the kidney,
the net result is to increase water reabsorption
o ADH acts on the collecting duct bc the collecting duct has receptors
for ADH
o When those collecting duct cells are stimulated, they increase in the
number of aquaporin 2 on the luminal membrane
o When you have more water channels in the luminal membrane,
more water is being reabsorbed
- You then excrete less water, meaning you are excreting less urine volume
- By doing this, you are conserving your body water
- Through feedback loops, hopefully the osmolarity of your ECF will go back
to normal
- If you are very depleted in body water, this conservation by ADH is not
enough – you need to behaviorally change (drink water)
o When ADH is in our blood, it also stimulates the thirst sensor,
making us thirsty
find more resources at oneclass.com
find more resources at oneclass.com
Blood Volume and ADH Release
- There are 2 inputs, blood pressure and blood volume
- We have other triggers that will synapse and affect those hypothalamic neurons
- Blood volume detectors in the atria and baroreceptors that will respond to MAP
- Those baroreceptors respond by sending less Aps to the solitary tract nucleus
- When we have less AP’s, that releases the inhibition so that we can now innervate the
hypothalamic neurons to release ADH
- So a decrease in MAP and a decrease in blood volume both cause an increase in ADH by the
posterior pituitary
- Similarily, once its in the blood, it travels to the body to have its affects but in the kidney its on
the collecting duct to increase the water reabsorption and decrease water excretion to conserve
blood volume
- Again, ADH will also make you thirsty so you drink fluid
- Negative feedback will take away the stimulation
- Once the volume returns to normal and the MAP returns to normal, the stimulation will be gone
Hypothalamic Integration of ADH Release
- Activating both osmoreceptors and baroreceptors leads to maximal ADH secretion
o Note: trigger for osmoreceptors is an increase in osmolarity
o Note: trigger for baroreceptors is a decrease in blood volume/BP
o So an increase in osmolarity and a decrease in BP will lead to maximal ADH secretion
- ADH only lives in the plasma for a few minutes so it has to be constantly made in order to
continuously produce maximal ADH in the blood
- What if these two inputs opposed each other?
o So what if instead you had a decrease in plasma osmolarity and a decrease in blood
volume?
▪ Osmoreceptors are more important during normal physiological conditions so
usually the body is more concerned with the osmolarity of the plasma than it is
with the BP or blood volume with the two things opposing in regards to ADH
release
▪ So in this case you would make a little less ADH
o So if you had an osmolarity that increased (which is the good signal) and the volume
was increased, the ADH amount would not increase
o What if you are hemorrhaging?
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Adh has a very short plasma life (couple of minutes) so in order for it to continue doing its job reabsorbing water, you need constant adh being released into the blood. The higher the concentration of adh, the more water will be reabsorbed by the collecting duct. Plasma osmolarity can change a lot from day to day. If you decide you are going to drink 1l of water, you will change your plasma osmolarity by 7- So if you"re an avg 70kg individual, its about a 7-8mosm change. The change in osmolarity is very detectable your neuroendocrine cells will start responding by. So it"s a very small, sensible, detectable change. Osmolarity, in the normal range, is the most important factor most sensitive input that these. Recall: osmolarity is detected by osmoreceptors (neurons that are found with and around the releasing more or less adh at 1-2mosm differences hypothalamic neurons will receive hypothalamus)
