Regulation of osmolality Flashcards
Where is ADH made
Supraoptic (SO) and Paraventricular (PVN) nuclei of the Hypothalamus
Where is ADH stored AND released from
Posterior pituitary
Half life of ADH and reason for it
~10 minutes
Levels can be rapidly adjusted depending on the body’s need for water conservation
What is the primary control of ADH
secretion
Plasma osmolality
What happens to ADH secretion when osmolality increases
Secretion increases
What is osmolarity
The concentration of a solution expressed as the total number of solute particles per litre
What happens in brain when plasma osmolality increases
The rate of discharge of ADH-secreting neurones in the SO and PVN is increased
Which increases the release of ADH
What receptors mediate neuronal discharge and where are they located
Osmoreceptors
Anterior hypothalamus near SO and PVN
What changes the discharging of osmoreceptors
Their volume (stretch-sensitive ion channels)
Normal plasma osmolality
280-290mOsm/kg
What does a small change in osmolality produce in regards to ADH
Rapid and marked change in ADH levels
System has a very high “gain” a 2.5% increase in osmolality can produce a 10x increase in ADH.
Is urea an effective or ineffective osmole
Ineffective
Why do hypertonic solutions, like seawater, lead to dehydration
They require more water to excrete them, due to high solute levels, than one gains water from their ingestion
What is the difference between tonicity and osmolarity
osmolarity takes into account the TOTAL concentration of PENETRATING solutes AND NON-PENETRATING solutes, whereas tonicity takes into account the total concentration of ONLY NON-PENETRATING solutes.
What is tonicity
The total concentration non-penetrating solutes
ADH AKA
Vasopressin
Where does ADH bind and what happens when it does
Binds to membrane receptor on collecting ducts
Receptor activates cAMP second messenger system
Causing more aquaporins to be inserted into the luminal membrane
Which increases the membrane’s water permeability
How permeable are the collecting ducts membrane’s to urea
Relatively, particularly towards the tips
ADH’s effect on late medullary collecting ducts
Increases permeability to urea
What happens to urea in an anti-diuresis with high levels of ADH, why and what is the consequence of it
urea is retained
To save water and reinforce medullary gradient in region of the ascending limb
Uraemia occurs.
Effect of increased ECF volume of [ADH]
Reduces [ADH]
Effect of decreased ECF volume on [ADH]
Increases [ADH]
Where a low P receptors found and what’s there other name
Left and right atria and great veins
AKA volume receptors
What are the high P receptors
The carotid and aortic arch Baroreceptors
What do moderate decreases in ECF volume 1° effect and cause
Atrial receptors
Decreased atrial receptor discharge therfore increased ADH secretion
When do carotid and aortic arch Baroreceptors affect ADH secretion
When the volume change is enough to affect the MBP
Does changing posture affect ADH secretion
Yes
Standing up from lying down cause increased ADH levels
What stimuli can increase ADH levles
Pain Emotion Stress Exercise Nicotine Morphine.
What stimuli can decrease ADH levels
Alcohol
ADH levels after traumatic surgery
Inappropriate levels, need to be careful monitoring water intake
Effect of Peripheral Diabetes Insipidus on collecting ducts
Insensitive to ADH
How can the areas that produce ADH be damaged, what does this cause and how is it treated
Tumour, surgery or meningitis
Central Diabetes Insipidus
ADH replacement
