Regulation of Osmolarity Flashcards
Water regulation is controlled by…
ADH/Vasopressin
What is ADH?
A 9 amino acid chain polypeptide hormone made in the supraoptic and paraventricular nuclei of the hypothalamus and released from the posterior pituitary gland
What is the 1y control of ADH secretion?
Plasma osmolarity - when this increases the rate of ADH discharge also increases
What are changes in neuronal discharge of ADH mediated by?
Osmoreceptors in the anterior hypothalamus - close to the supraoptic and paraventricular nuclei
What other receptors are there in the lateral hypothalamus?
Ones that mediate thrist
How do osmoreceptors work?
If osmolarity increases, H2O leaves the cell causing it to shrink and activate stretch sensitive ion channels
This increases neural discharge which increases ADH secretion
If osmolarity decreases, cells swell and neural discharge decreases
So changes in the BLANK of the osmoreceptors leads to changes in…
Volume
Leads to changes in osmoreceptor discharge
What is normal plasma osmoLALity?
280-290 mOsm/kg H2O
It is very precisely regulated
What happens if small changes in plasma osmolality occurs?
Leads to rapid changes in ADH
Even a 2.5% increase in osmolality leads to 10x more ADH
If osmolarity increases but tonicity doesn’t - does this still entice a ADH response? Explain
No - because solutes that penetrate membranes without need of transporters move together with water and do not create any osmotic drag like ions do
Give examples of a substance that changes osmolarity but not tonicity.
Urea can move in and out of the cell changing osmolarity but it doesn’t create any water gradients so tonicity stays the same
Is the concentrating ability of the kidney high or limited? What does this mean for the amount of urine produced?
Limited
The amount of urine produced depends not only on the [ADH] but also on the amount of solute to be excreted
If 2400 mOsm of solutes needed excreted, how much urine would need to be made to get rid of this?
Even at max concentrated urine - 1200/1400 you would need at least 2L to get rid of it
So why is ingestion of hypertonic solutions dangerous? Give an example.
Leads to rapid dehydration as the body needs to get rid of these extra solutes via urine
Drinking seawater will cause to to increase urine flow to get rid of salt meaing you excrete more water to do so and you will die of dehydration
How does ADH work?
Binds to membrane receptors in the collecting duct which activates aquaporins increases permeability of H2O
This allows the CORTICAL collecting duct to become equilibrated with the interstitial at 300 mOsm/L
The collecting duct then passes through the hypertonic medullary interstitial gradient and water is removed or retained as needed, dictated by ADH
What happens in the hypertonic medullary area if max. ADH is present?
then the contents equilibrates with the medullary interstitium with water with moving out making the collecting duct contents highly concentrated at the tip of the medulla
How is H2O reabsorbed from the interstitium?
By the oncotic pressure of the vasa recta
What happens to oncotic pressure in the vasa recta if there is a H2O deficit in the body?
Will be greater to = more reabsorption
What happens in the absence of ADH?
Collecting ducts are impermeable to H2O and it is excreted as waste
Further ions can be reabsorbed from the collecting ducts leaving urine osmolarity sometimes at 30-50!!!
What is the role of urea?
In the presence of ADH - when water moves out of the collecting duct - it concentrates urea levels.
SO when urea approaches medullary tips it leaves the collecting ducts down its conc. gradient and gets reabsorbed which helps reinforce the interstitial gradient in the loops of henle area
What would happen if urea was not reabsorbed?
Would exert an osmotic effect and hold water in the collecting ducts stopping rehydration
If urea is a waste product why is it reabsorbed?
The conservation of water is more important than any effects of high urea
What else besides plasma osmolarity affects ADH secretion?
ECF volume
An increase in volume = a decrease in ADH and vice versa
An inverse relationship exists between…
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.
Low P receptors are located in….
L and R atria and great veins
What are L pressure receptors often called? Why?
Volume receptors because they monitor the return of blood to the heart and the “fullness” of the circulation.
Where are high P receptors located and what are they called?
Carotids and aortic arch
baroreceptors
What are moderate decreases in ECf volume picked up by?
The low P atrial receptors
Normally they exert a tonic inhibitory discharge of ADH secreting neurons via the vagus nerve
But ECF volume decreases, the activity of atrial receptors decreases and ADH is released
If volume changes are enough to change mean BP - what is the system to correct this? When is this particularly important
Carotid and aortic receptors will also contribute to changes in ADH secretion
Drop in BP increases ADH
Very important in haemorrhage
What are some other stimuli affecting ADH?
Increases in - pain, stress, morphine. Following traumatic surgery inappropriate ADH secretion can occur
Decreases with alcohol
Recap the 3 main things that stimulate ADH release.
Osmolarity greater than 280-290
Decrease in atrial stretch due to low blood volumes
Decrease in BP
What is diabetes insipidus?
An ADH deficiency
Causes of central DI?
Hypothalmic damage or disease (surgery, tumours or meningitis)
Causes of peripheral DI?
Collecting duct insensitivity
Characteristics of DI?
Very large volumes of very dilute urine = polyuria
Polydipsia
How to treat central DI?
Give ADH
How can peripheral DI be managed?
Cannot give ADH so must be managed via the thirst mechanism
Treat the cause if known
What are some causes of peripheral DI?
Usually 2y to hypercalcaemia or hypokalaemia
