Regulation of Osmolality Flashcards
What hormone controls water regulation at the kidneys? Where is it synthesized? How responsive is it to the bodies needs for water reabsorption?
- ADH / Vasopressin / AVP
- Synthesized by hypothalamus, secreted by posterior pituitary
- Has a half life of about 10 mins so conc. can be rapidly adjusted to meet body needs
Which nuclei in the hypothalamus of the brain are responsible for ADH production?
- Supraoptic (SO) nuclei
- Paraventricular nuclei (PVN)
What initiates the release of ADH from the posterior pituitary?
- Osmoreceptors in the anterior hypothalamus detect hypertonicity (high substrate conc.) of the plasma
- ECF volume
(Other receptors in the lateral hypothalamus mediate thirst)
How do the osmoreceptors in the anterior hypothalamus detect changes in the osmolarity of plasma?
- If plasma osmolarity is high, water is drawn out of osmoreceptors causing the cell to shrink, this activates stretch sensitive ion channels causing ADH release
- If osmolarity is low, water moves into the cells causing them to stretch, which reduces ADH secretion
What is the normal plasma osmolarity? How sensitive is the ADH system at regulating it?
- Normal: 280-290 mOsm/Kg
- Very sensitive, a 2.5% increase in plasma osmolarity can produce a 10x increase in ADH
Why can an increase in plasma osmolarity sometimes not produce an increase in ADH secretion?
- Because some solutes increase osmolarity but not tonicity, because they can penetrate membranes
- If a solute is lipid soluble it will diffuse into osmoreceptor cells, so the osmolarity of the cell compared to the plasma will remain the same (isotonic)
Why does salt water make you dehydrated?
- Because the ingestion of hypertonic solutions means more water is needed to excrete the solute than was ingested with it
- If you ingest 1L of 2400mOsm solution, even with max. urine conc. (1200mOsm), you’d need to produce 2L of water to excrete the solute
How does ADH increase water reabsorption?
Binds with receptors on the surface of collecting duct cells, causes the recruitment of H2O channels (aquaporins) to the collecting duct cell surface
- Allows passage of H2O into collecting duct cells, and then out into the medullary ISF where it can be reabsorbed into the vasa recta
What happens to the concentration of the collecting duct contents when there is maximal ADH?
- It equilibrates with the concentration of the medullary interstitium, water is allowed to flow out of the CD freely and so flows into the concentrated interstitium, where the vasa recta reabsorb it
- This leaves the concentration of the urine equal to that of the interstitium (1200 mOsm)
When maximal ADH is present how effective are the vasa recta at absorbing the water let out by the collecting duct?
The amount of ADH is proportional to the osmolarity of plasma, therefore when ADH is maximal the oncotic pressure drawing water into the hypertonic plasma will be very high
What happens to the concentration of urine in the collecting duct when there is no ADH?
- The collecting duct wall is impermeable to water when there is no ADH, so the medullary interstitium is ineffective at drawing water out of the duct
- This means the urine remains a low osmolarity from the top to the bottom of the duct, and there is excretion of dilute urine
How is the concentration of urea affected by maximum ADH concetration?
- Maximum ADH causes water to move out of the collecting duct, concentrating the urea
- The CD is relatively permeable to urea though, particularly at the medullary tips where [urea] is high
- So with max. ADH urea will flow with its conc. gradient out to the interstitium at the medullary tips, which reinforces the interstitium gradient to save water
What is a complication of the movement of urea into the interstitium when maximum ADH is present? What are the benefits?
Complication is uraemia
Benefit is the maintenance of the interstitium gradient which allows the reabsorption of water
The conservation of water is more important than the retention of urea
How does ECF volume effect ADH secretion?
- High ECF volume causes a decrease in ADH secretion
- Low ECF volume causes an increase in ADH secretion
Inversely proportional
What receptors detect changes in ECF volume, causing changes in ADH secretion?
- Low pressure receptors in the left and right atria, as well as in the great veins
- High pressure receptors in the carotid and aortic arch baroreceptors
