Regulation of Osmolarity Flashcards
What hormone is responsible for water regulation
ADH (vasopressin)
What is the hormone ADH composed of
A polypeptide hormone, composed of 9 amino acids
Where is the ADH hormone, synthesised and stored
synthesised in the supraoptic (SO) and the paraventricular nuclei (PVN) of the hypothalamus in the brain
Stored in Posterior pituitary hormone
Why is the Half life of ADH 10 minutes
So can rapidly be adjusted depending on the body’s needs for H2O
What does control of ADH secretion depend upon
Plasma osmolarity (primary control)
ECF volume
What is normal plasma osmolarity
280-290mOsm/kg H2O
How does increased plasma osmolarity increases ADH secretion
Due to osmoreceptors
as high osmolarity, causes water to move out the osmoreceptor cells, causing them to shrink activating the stretch sensitive ion channel, increasing neural discharge, stimulating the release of ADH from the posterior pituitary
Where is the osmoreceptors located
Anterior hypothalamus
What specifically does the osmoreceptors sense
The effective osmotic pressure which is a measure of tonicity, which creates the osmotic drag allowing what osmotic receptors cells to either shrink or expand due to water movement in or out the cell
What effect does decreased plasma osmolarity, have on osmoreceptors
A decreased osmolarity means that water moves into the cells of the osmoreceptors causing them to swell decreasing the neural discharge therefore decreasing ADH secretion
How is the plasma osmolarity regulated very precisely
Corrected very quickly and very sensitive to change
as a small change in the plasma osmolarity produces a very strong response to ADH
What is the relationship between ECF volume and ADH secretion
Inverse relationship
Increased ECF volume causes a reduced ADH secretion
What mediates the relationship between ECF volume and ADH secretion
Low and High pressure receptors
Where are low pressure receptors found
Found in left and right atrial
and great veins
Where are high pressure receptors found
Is the carotid and aortic branch baroreceptors
What is the purpose of low pressure receptors
Are volume receptors, monitoring the return of blood from the heart
Normally exert tonic inhibitory discharge of ADH secreting neurones via vagus nerve
What is the affect on low pressure receptors when ECF volume moderately decreases
ECF volume decreases, decreases atrial receptor discharge of inhibitory vagal block therefore increase ADH release
When are high pressure receptors affected in the relationship with ECF volume
High pressure receipts are affected when the volume changes enough the affect the mean blood pressure
When would high pressure receptors trigger the release of ADH
When the ECF volume has decreased enough the decrease BP, decreasing the receptor discharge of the high pressure receptors, resulting in the release of ADH
When are high pressure receipts triggered
When going from lying down to standing up - slight increase in ADH release
Very important in haemorrhage
What other stimuli increases ADH release
Pain emotion stress exercise nicotine morphine following traumatic surgery inappropriate ADH secretion monitoring H2O intake
What stimuli decreases ADH release
Alcohol surpasses ADH release
Where is the site of water regulation
The collecting ducts
How does ADH control water regulation in the collecting ducts
By affecting the permeability of the collecting ducts to water reabsorption
What does the amount of urine produced depend upon
The concentration of ADH and also the amount of solute to be secreted (so whether the filtrate urine delivered to the tubule is concentrated)
What occurs in the collecting ducts when ADH is present
The collective ducts become permeable to water and H2O is able to leave the collecting ducts
What drives the reabsorption of water from the collecting ducts
It is driven by the hypertonic medullary interstitial gradient, created by the countercurrent multiplier of the loop of Henle.
What occurs once water is reabsorbed from the collecting ducts
The cortical collecting duct becomes equilibrated with that of the cortical interstium (300mOsm)
H2O is then absorbed by the vasa recta
What occurs when a maximum concentration of ADH is present at the collecting ducts
The collecting duct contents equilibrates with that of the medullary interstium via the reabsorption of water therefore collecting duct contents becomes highly concentrated at the tip of medulla
therefore producing a small volume of highly concentrated urine
When is there a maximum concentration of ADH at the collecting ducts
When you are compensating for water deficit and want to reabsorb as much H2O as possible
In maximum ADH concentration, what happens to the water reabsorbed
You are effectively adding pure H2O to the ECF, which is then reabsorbed by the oncotic pressure of the vasa recta which is greater that usual in the presence of H2O deficit
What does the presence of ADH cause a secondary affect to
Urea reabsorption
How does increased ADH cause an increased urea reabsorption
The reabsorption of water from the collecting ducts, concentrates the remaining urea in the collecting ducts
and as the collecting ducts as particularly permeable to urea at the medullary tip
as urea approaches the medullary tip, due to its high concentration, there is a tendency for it to be reabsorbed
What is the purpose of urea reabsorption, as a secondary affect of ADH
It is important that urea should be reabsorbed because if it remained in the tubule, it would exert an osmotic effect to hold H2O in the tubule
Also reinforces the medullary gradient in region of thin ascending limb
What does continually reabsorption of urea cause
Ureamia syndrome
What occurs in the absence of ADH in the collecting ducts
In absence the collecting ducts are impermeable to H2O, so the medullary interstitial gradient is ineffective in inducing H2O movements out of the collecting ducts
therefore large volume of dilute urine is excreted
When would there be an absence of ADH
When compensating to water excess, as osmolarity can fall to 30-50mOsm (basically excreting pure water)
What is the normal level of ADH
Any level of ADH between the extremes of [max] and absence is possible, so that the Collecting duct permeability can be precisely graded to meet the demands of the body for H2O regulation.
How does ADH increase the permeability of the collecting ducts
By incorporating H2O channels (aquaporins) into the luminal membrane
What occurs when ADH stimulates increased permeability of collecting ducts
ADH indicated signaling cascade the tell lipid vesicles in collecting duct cell storing the aquaporin to fuse to the membrane in the side of the collecting duct
increasing the number of aquaporins in the luminal (apical)membrane
What occurs in ADH signalling cascade in the collecting duct cell
ADH binds to membrane receptor activating cAMP second messenger system,
What needs to be present on collecting ducts for water to be reabsorbed
Aquaporin
What condition is associated with ADH hormone deficit
Diabetes inspidus
what are the two types of diabetes insipidus
Central DI - problems with producing ADH
Peripheral DI - collecting ducts may be impermeable to ADH
What is the potential causes of central DI
The hypothalamic areas synthesizing ADH may become diseased due to tumours, or in meningitis.
They may be “damaged” during surgery
What is the causes of peripheral DI
Usually secondary to hypercalcemia and hypokalaemia
Genetic defects in ADH receptors
Defect in genes for aquaporins
What is diabetes inspidus characterised by
passage of very large volumes of very dilute urine, generally > 10 l/day = polyuria
They drink large volumes of H2O = polydipsia.
What is the treatment for diabetes inspidus
Central: Give ADH (AVP)
Peripheral: Manage thirst
Treat underlying cause
cant give ADH
