Flashcards in Regulation of Osmolarity Deck (23):
What is water regulation controlled by?
What is ADH?
Polypeptide (9amino acids)
Synthesised in the supraoptic (SO) and paraventricular (PVN) nuclei of the hypothalamus in the brain.
Posterior pituitary hormone
WHat is the half life of ADH?
So can be rapidly adjusted depending on the body's needs for H2O conservation
What is the primary control of ADH secretion?
When the EFFECTIVE osmilarity of the plasma increases the rate of discharge of ADH- secreting neurones in the SO and PVN is increased
Increased release of ADH from the posterior pituitary
What receptors detect incraesed plasma osmolarity?
Osmoreceptors in the anterior hypothalamus, close to the SO and PVN.
Other receptor in the lateral hypothalamus mediate thirst.
How do osmoreceptor work?
-Incaresed H2O outside cell
-Cell shrinks/ stretch sensitive ion channel activated
-Incraesed neural discharge
-Incraesed ADH secretion
-H2O enters and cell swells
-Decreased neural discharge
-Decreased ADH secretion
What is normal plasma osmolarity?
It is regulated VERY precisely
Small changes in either direction results in rapid changes in ADH.
System has a very high "gain" a 2.5% increase in osmolarity can produce a 10x increase in ADH.
What do we mean by effective osmolarity?
Osmolality is a measure of the number of particles present in solution and is independent of the size or weight of the particles. It can be measured only by use of a property of the solution that is dependent solely on the particle concentration.
Tonicity is the effective osmolality and is equal to the sum of the concentrations of the solutes which have the capacity to exert an osmotic force across the membrane.
Is urea tonic?
Does it have an effective osmolarity?
Urea can pass through most cells. So will equilibriate
Concentration of urea in ECF relative to intracellular fluid doesnt change.
No water movement so no tonicity.
What does the amount of urine produced depend on?
Amount of solute to be excreted.
Whay does the amount of solute to be excreted effect the amount of urine we must produce?
If the amount were 2400mOsm, then even with maximally concentrated urine (1200-1400mOsm/l), this would mean excretion of 2L of urine.
Limit on concentration so more solute = more water
This is why you cant hydrate with salt water. Have to excrete salt and will always excrete more than you gain.
How does ADH increase the permeability of collecting duct cells to water?
ADH receptor causes storage vesicles to deposit H2O channels into the apical membrane.
These H2O channels are called aquaporins
How does the collecting duct continue to reabsorb water past normal plasma levels?
Collecting duct becomes equilibriated with the cortical interstitium (300mOsm/l)
Then the collecting duct passes through the hypertonic medullary interstitial gradient, created by the countercurrent multiplies of the loop of Henle
How does the absence of ADH effect water reabsorption?
Collecting ducts are impermeable to H2O, so that the medullary interstitial gradient is ineffective in inducing H2O movements out of the collecting ducts and therefore a large volume of dilute urine is excreted, compensating for H2O excess.
What is the most dilute urine you can produce?
Since further ions are reabsorbed from the collecting duct in addition to maximum reabsorption urine osmolarity can fall to 30-50mOsm/l
What is the role of Urea in producing concentrated urine?
In the presence of ADH, movement of H2O out of the colleccting ducts greatly concentrates the urea remaining in the ducts.
Collecting duct membranes are relatively permeable to urea, particularly towards medullary tips.
So as urea approaches the medullary tips, there is an increased tendancy for it to move out down its concentration gradient.
The permeability of the late medullary CD to urea is enhanced by ADH.
So in antidiuresis with high levels of ADH, urea will be reabsorbed from the collecting duct into the interstitium
How does ECF volume affect ADH secretion?
Increase in ECF volume = decrease in [ADH]
Decrease in ECF volume = increase in [ADH]
Inverse relationship between the rate of ADH secretion and the rate of discharge of stretch receptor afferents in the low and high P areas of the circulation
Where are stretch receptors found in the circulation?
Low P receptors are located in the L and R atria and great veins.
Sometimes called "volume receptors" because they monitor the return of blood to the heart and the "fullness" of the circulation
High P receptors are the carotid and aortic arch baroreceptors
Moderate decreases in ECF volume primarily effect what receptors?
Normally they exert tonic inhibitory discharge of ADH secreting neurones via the vagus nerve
Decrease ECF volume ->
Decrease atrial receptor discharge ->
Incraesed ADH release
Volume changes enough to effect MBP effect what receptors?
Carotid (and aortic) receptors will also contribute to changes in ADH secretion
Very important in haemorrhage.
Even when going from lying down to standing up, there is an increased ADH release
The inverse of these changes occur on volume expansion
What other stimuli may increase ADH release?
Following traumatic surgery -> inappropriate ADH secretion occurs -> monitor H2O intake and output
What may damage hypothalamic areas leading to cranial diabetes insipidus?