Lecture 29: Renal 3: The Role Of Kidneys In Water Balance Flashcards
Describe osmolarity and describe how osmolarity affects water movement in the body
-osmolarity is a measure of the total number of solutes in a solution (measured in mOsmoles/L)
-osmolarity is the inverse water concentration
-osmosis= water movement across semi permeable membrane.
-water will move from high water concentration (= low osmolarity) to low water concentration (=high osmolarity)
-water will move until the water concentration and osmolarity eps are equal = osmotic equilibrium
-water moves through cell membranes through channels known as aquaporins
With impermeable particles only water can move
Give an overview I’d water balance in the body.
Also why do we regulate water?
Water gain: food and drink and metabolism (2.5L A day)
Water loss: skin, lungs, urine and faeces (2.5L a day)
Why?
-to maintain body water, blood volume and blood pressure
-to maintain osmolarity of body fluids
Changes to osmotic equilibrium.
Describe how these changes would affect osmolarity?
1. Drinking of pure water
2. Consumption of salty chips
- Drinking of pure water
- osmolarity of ECF decreases, water flows into cells, cells swell. Increased volume, same solutes - Consumption of salty chips
- osmolarity of ECF increases, water flows out of cells, cells shrink.
Swelling or shrinking of brain cells causes confusion, coma and death. Kidneys help avoid this situation by changing the rate of water reabsorption and excretion.
Check out slide 7 of water handling in kidneys
Describe the sites of synthesis and secretion of ADH and the factors that affect its secretion.
-peptide hormone that regulates water reabsorption on the distal tubule and collecting ducts. Produced: hypothalamus Stored and secreted: posterior pituitary gland Released into blood in response to osmotic and baroreceptor signals. Factors affecting ADH secretion: Stimulation: -increased ECF osmolarity -low blood volume -decreased mean arterial pressure -⬆ temperature -stress (pain, exercise) -nausea and vomiting -angiotensin 2 -nicotine and ecstasy
Inhibition:
- decreased ECF osmolarity
- high blood volume
- increased mean arterial pressure
- ⬇ temperature
- alcohol
Osmolarity changes are detected by osmoreceptors in the hypothalamus are the most important signals for changes in ADH secretions. Only large changes in blood volume will affect it
Osmoreceptors and ADH
Small changes in osmolarity can lead to significant changes in ADH secretion
- ⬆osmolarity➡ ⬆ ADH secretion➡⬆water reabsorption in kidneys
- ⬇osmolarity ➡⬇ADH secretion ➡⬇ in water reabsorption in kidneys.
Baroreceptors and ADH
-need changes of >10% to get significant changes in ADH secretion
-change in BP detected. H baroreceptor a in carotid and aortic arch,
-changes of blood volume detected by volume receptors in atria.
-⬇BP/volume ➡⬆ADH secretion➡⬆ water reabsorption in kidneys
-⬆B/volume ➡⬇ADH secretion➡⬇ water reabsorption in kidneys
Note: that the kidneys can’t bring blood volume back to normal, only reduce further loss
Slide 11
Cellular action of ADH (vasopressin)
- ADH binds to receptors on basolateral membrane of principal cells on distal tubule and collecting duct.
- Receptor activates cAMP 2nd messenger syste,
- Cell inserts water channels (Aquaporins) in luminal membrane.
- water channels are always present in basolateral membrane. - Water is absorbed by osmosis into the blood
When ADH is present, water is reabsorbed through the tubular epithelial cell IF there is an osmotic gradient
The loop of Henle establishes this osmotic gradient
How does ADH conserve water?
By concentrating the urine volume.
This is achieved by:
-setting up large osmotic gradient in the medullary interstitial fluid
-large amounts of water then reabsorbed from the collecting ducts.
The osmotic gradient in the interstitial fluid is set up by the loope of Henle
By a mechanism know as the countercurrent multiplier
What are the essential points in countercurrent multiplier mechanism
- descending limb is freely permeable to water, not to solutes, so water reabsorption but no solute reabsorption.
- ascending limb is impermeable to water, active reabsorption of NaCl into interstitial fluid. Solute reabsorption but no water reabsorption
- distal tubule and collecting duct ate permeable to water if ADH is present.
Check out slide from 16-19 on setting up the osmotic gradient
- The active salt up in th ascending limb establishes a 200 mOsm gradient at each horizontal level
- As the fluid flows forward several “frames” a mass of 200 mOsm of fluid exits into the distal tubule and a new mass of 300 mOsm fluid enters from proximal tubule
- The ascending limb pump and descending limb passive fluxes resstablishing the 200mOsm gradient at each horizontal level.
- Once again the fluid flows forwards several frames
- The 200 mOsm gradient at each horizontal level is established once again
- The final vertical osmotic gradient is established and maintained by the ongoing countercurrent multiplication of the long loops of Henle
What happens in the absence of ADH?
No vasopressin present so distal tubule and collecting duct are impermeable to H20. So a large volume of dilute urine is excreted, no H20 is reabsorbed in distal portion of nephron; excess H20 is eliminated from the body in urine.
Tell me about obligatory water loss
Is the minimum volume of Horne that must be excreted to eliminate solutes remaining in tubular fluid.
- not all solutes in tubular fluid are reabsorbed
- a minimum amount of water has to be excreted to assist in solute/waste movement
- the obligatory water loss is determined by the maximum con enacting ability of our kidneys
What is the role of urea in concentrating urine?
- not all the osmolarity of the medullary interstitial fluid is due to NaCl
- reabsorbed urea constitutes about 40%
- urea is a waste product of protein (amino acid) metabolism
- so a low protein diet reduces our ability to concentrate the urine eg protein malnutrition, starvation, infants.
Describe some of the disorders of ADH and urine concentration
Diabetes insipidus:
Can be central or nephrogenic
Another disorder is syndrome of inappropriate secretion of ADH
Diabetes insipidus is increased urine volume, strong thirst, sever risk of dehydration
Central: failure to produce ADH
- head injury
- meningitis
- congenital
Nephrogenic= failure of kidneys to concentrate the Rhine in response to ADH
- congenital eg mutation to ADH receptor
- failure to produce an adequate osmotic gradient in medullary intertitium due to drugs
Another disorder is syndrome of inappropriate secretion of ADH
- excess ADH
- reduced volume of concentrated urine
- Hypotonic plasma and osmotic swelling
- causes:
- ADH producing tumours
- drugs eg ecstasy
