Osmoregulation Flashcards
All body fluids, expect the interstitial space of the renal medulla have an osmolality of ………
285m mosm/kg
What contributes to body fluid balance?
intake - food, drink, metabolism
losses - respiration, insensible water loss through skin, faeces
Describe the control of ADH release
- where is osmolality detected?
- where is ADH synthesised and released from?
- what is the half-life of ADH?
- osmolality is detected int he arterioventral third ventricle (AV3V) region, where the BBB is incomplete
- AV3V neurones project to the supraoptic and paraventricular parts of the hypothalamus
- thy repsond to an increase in osmolality by increasing the release of ADH from the posterior pituitary
- ADH is synthesised in the cell bodies in the form of a pre hormone, cleaved as it descends to the pituitary
- ADH co-rereleased with its carrier peptide neurophysin (function unknown)
- ADH is unstable in the circulation, and so only has a half-life of 10 min
What are the main receptors that ADH acts on?
Where are they located?
What signalling pathway do they use?
What are the effects of ADH here?
- V2 receptors
- on the cortical collecting ducts, basolateral membrane
- adenylyl cyclase –> PKA –> exocytosis of vesicles containing AQP2. Also acts to increase transcription of AQP2
- this increase permeability of collecting ducts to water so the urine becomes more concentrated
What are the secondary receptors for ADH?
Where are they located?
What is their signalling pathway?
What are the effects of ADH here?
- V1 receptors
- smooth muscle cells of veins
- signal via PLC(IP3/DAG)
- this causes venoconstriction (important as ADH is stimulated to be released when plasma osmolality is high, mean plasma volume may be low, venoconstriction therefore helps to maintain blood pressure)
Describe the structural organisation of AQP1
multisubunit oligomer organised as a tetramer of four identical subunits with a large glycan attached to only one
What is the hypothesis of oxytocin?
What 3 things do we know about oxytocin?
Hypothesis: oxytocin triggers thirst
- oxytocin is a key trigger of the milk let-down reflex
- oxytocin is also an agonist at V1 and V2 receptors
- breast feeding commonly triggers thirst
How is thirst triggered?
- inadequate water intake causes an increase in osmolality of the plasma
- as for the regulation of ADH release, osmolality is detected in the anteroventral third ventricle (AV3V) region
- AV3V neurones project to the median preoptic area of the hypothalamus, which increases thirst
What are is the body’s response to ‘binge’ drinking water
decreased osmolality causes a suppression of ADH release and suppression of thirst. This suggests, correctly, that there is tonic ADH release
What is the urine production rate and urine osmolality in the following situations:
- maximal ADH
- no ADH
Max ADH - production rate = 300-400ml/day - osmolality = 1300mOsm No ADH - production rate = 25L/day - osmolality = 60-90mOsm
What is the effect of drinking sea water?
Use calculations to explain your answer.
Osmolality = 2000mOsm
To clear 1kg of sea water will require 2000/1400mOsm of water to clear
Why is it really important to not make formula feeds for neonates too concentrated?
neonates can only produce osmolality of 500mOsm.
Not all dietary osmolites are equal.
What are the dominant osmolytes?
Na+ and K+
Do carbohydrates contribute to osmolality? Why?
Carbohydrates
- converted to simple sugars, are transported into cells, so don’t contribute significantly to osmolality
- except in diabetes mellitus
- glucose in cells is oxidised to CO2 and water so only transiently increases osmolality
Do proteins contribute to osmolality? Why?
Proteins
- broken down into AA’s, transported into cells, plasma change is osmolality is small
- nitrogen is removed through urea, which has a high renal clearance; so while the flux is high, the contribution to osmolality is low
