Water Balance Flashcards
LEARNING OUTCOMES
- Where in the nephron is water managed
- What is the mechanism
- How is it controlled
2 routes to water loss
- Via kidneys
- Insensible water loss
How much urine must we output per day
500 ml, even in situations where we are seriously dehydrated we still must output this to get rid of waste products
What is the upper limit of water loss
18L per day - 10% of GFR
What is insensible water loss
Loss of water from skin and lungs - can be as high as 3.5L/hr from skin during exercise in hot conditions
Water input

Water output

Water input =
Water output, despite variable water intake
How does the body measure our salt requirement
Based on changes in EC fluid vol and pressures
How does the body measure our water requirement
Through ECF osmolarity
- If ECF osmolarity is high than we are water STARVED and need to save and source water => thirsty
- If ECF osmolarity is low than we are water RICH and need to remove water => pee more
NOTE: under normal circumstances osmotic pressure inside and outside the cell is =
Name and explain the 3 ways we measure water in the body
- OSMORECEPTORS - sense Posm, located in the Paraventricular Nucleus (PVN) in the brain
- [PADH] - feedback mechanism regulated by changes in receptor activity
- DISTAL NEPHRON - ADH responsive cells CNT and P cells
Normal osmolarity
280-300 mOsm/L
Function of ADH
Where is it produced
Acts against water loss/promotes the saving of water
Produced by neurons in the PVN
When do osmoreceptors fire
Above 290 mOsm/L, triggering the release of ADH
Impact of an increase in ECF osmolarity on cells
An increase in ECF osmolarity => cells shrink, sending more APs triggering release of ADH
Impact of a decrease in ECF osmolarity on cells
A decrease in ECF osmolarity => cells swell, sending less APs and the release of ADH is suppressed
Osmolarity and ADH
- High osmolarity triggers ADH release and ADH promotes the saving of water by the kidney
- Low osmolarity stops ADH release and water is lost by the kidney
Alternative names for ADH
AVP (Arginine Vasopressin) or VP (vasopressin)
=> ADH promotes vasoconstriction (vasopressive properties)
Why might ADH need to save water
- Osmolarity is high
- ECF volume is low
In both cases saving water is good and helps the situation but when ECF vol is low, vasoconstriction will help to support BP and thus ADH has 2 roles depending on the reqs to fix water or pressure or both
The body can manage these very quickly as ADH is produced very quickly and broken down very quickly in the liver - thus we get minute to minute control with ADH
Despite the presence of ADH, what is the problem
We have no water pumps
So before water can be saved and ADH can have any effect we need to create a water saving environment (which is made regardless of our water requirement)
Kidney works on the basis that we will need to save water at some point so be prepared and let ADH be the rapid response element in the process
Osmolarity at the glomerulus
300
Osmolarity at the PCT
300
Osmolarity at the tip of the LOH
1200
Osmolarity entering the DCT
100
Osmolarity at the DCT
100
Filtrate and interstitial osmolarity
Numbers reflect the osmolarity of the IS fluid bathing the capillaries and nephrons inside the kidney

What does the TAL of the LOH do
Actively pumps out salt

What does the TDL of the LOH do
Water is pulled out because the osmolarity of the IS fluid bathing the capillaries and nephrons is greater than the filtrate (enhanced by the unique arrangement of the LOH and medullary peritubular capillaries)

What supports a higher osmolarity in the IS fluid
Recycling of urea between loop and collecting duct
How do we create a hypertonic medulla
THE SINGLE EFFECT - pumping of salt out of the thick ascending limb
however this does not account for the large gradient so some other mechanism must be at play
What does countercurrent multiplication do
Magnifies the degree of hypertonicity to achieve 1200 mOsm
Countercurrent multiplication - how it happens
- Ascending limb starts to actively reabsorb salt (i.e. move salt out of the nephron and into the IS fluid spaces)
- As this process continues we see that the osmolarity of the fluid in the nephron in this region drops to 200 mOsm
- It drops because salt has been reabsorbed and water stays behind
- Meanwhile as salt is pumped into the IS fluid spaces the osmolarity here increases to 400 mOsm because we are adding salt
- As the descending limb of the LOH is permeable to water and the fluid in the IS fluid is at a higher osmolarity this pulls water out of the descending limb increasing its osmolarity

How does countercurrent multiplication continue
- Process repeats and the gradient builds
- However, would the fluid that leaves the descending limb not dilute the IS fluid and so return osmolarity to normal?
- Countercurrent multiplication does build a gradient but not a very big one
- VASA RECTA comes in to play

What is happening in this diagram

- Salt is pumped out of the thick ascending limb
- Some salt sits around in the IS space locally and more is picked up by the slow moving vasa recta which drags the salt towards the tip of the LOH
- As the vasa recta is slow moving and the flow is towards the tip the gradient builds up substantially with salt concentrating at the tip of the LOH
- WATER - as the ascending arm of the vasa recta rises with its salt-rich blood, it pulls water out of the descending LOH BUT because the flow of the vasa recta is up towards the cortex this water is being pulled away from the tip of the LOH ensuring the gradient is not diluted
VASA RECTA AND ITS INVOLVEMENT WITH THE GRADIENT
- net effect of the process on filtrate
- effect in IS fluid
- Fluid heading for the distal nephron is now of low osmolarity so rich in water
- Fluid next to the tip of the LOH is hyper osmotic (1200 mOsm) and the fluid nearer the cortex is isosmotic (300 mOsm)

What does the osmotic gradient mean
What happens as a result
We have a water rich solution in the distal nephron and on the other side of the nephron wall in the IS space we have a hyperosmotic fluid
This osmotic gradient encourages ADH to come in (recall - ADH is released when ECF osmolarity is high)
Presence of ADH

Facilitates the movement of water down its conc gradient, saving water for the body and the vol of urine produced is small
Urine will be of a high osmolarity and dark in colour

Absence of ADH

The movement of water down its conc gradient is blocked
Water is lost from the body and the vol of urine produced is large
urine will of a low osmolarity and light in colour

Osmolarity at each part of the nephron

How is ADH release influenced by osmolarity, blood vol and BP
- Osmolarity goes up when we need water - ADH goes to distal nephron - water is saved
- 1% increase in ECF osmolarity increases ADH
- 2% decrease below 280 mOsm/L decreases ADH to 0
- Blood vol goes down - we need more vol - ADH goes to distal nephron - water/vol saved
- BP goes down - we need more vol to support pressure - ADH goes to distal nephron - water/vol saved
Concept map 1

Concept map 2

Concept map 3
