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Lecture 41

Physiology 3120 Lecture Notes - Lecture 41: Posterior Pituitary, Osmoreceptor, Collecting Duct System


Department
Physiology
Course Code
PHYSIO 3120
Professor
Tom Stavraky
Lecture
41

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Lecture 41 Hormone Regulation of Water Absorption
Regulation of water balance
- Regulation of water balance is through one hormone, AD( either make it or don’t
- The volume of the extracellular fluid (ECF) is linked to blood pressure
o High fluid volume = increases blood pressure
- When ECF volume is decreased due to a decrease in total body water (have not ingested
enough fluid), Anti-diuretic hormone (ADH) is released
o Diuresis: increasing production of urine
o Drinking more water = causes diuresis (produce more urine)
o Diuresis = diuretics = imbalances
o There are diuretics (drugs) that make you produce more urine than you should,
making you dehydrated
o Diuresis means increased urine production
o Anti-diuresis = decreasing urine production
- ADH REDUCES URINE PRODUCTION BECAUSE YOU WANT TO CONVERSVE WATER LEVELS
- Decrease in ECF fluid volume is one of the ways that our body releases ADH
- ADH made by neuroendocrine cells in the hypothalamus
o Hypothalamus has neurons that project to and make the posterior pituitary
o Cell bodies of the neurons are located in the hypothalamus and they make ADH
- Vesicles with ADH are stored in the posterior pituitary
o ADH is stored in the axon terminals of the nerves (location in posterior pit)
- Peptide hormone
- Triggered for release by low ECF volume, high plasma osmolarity and angiotensin II
o Not having enough body water = higher solutes
o Integration between sodium and water balance with ang II
- Sensed by baroreceptors and osmoreceptors
o Volume changes detected by baroreceptors
o Osmoreceptors detect osmomolarity
- Baroreceptors:
o Located in aortic arch and carotid sinus (low blood pressure detection)
o Also volume receptors in atria
o When blood pressure and volume decreased, less action potentials are sent to
hypothalamus = ADH released from neuroendocrine cells in posterior pit
- Osmoreceptors:
o Neurons that detect osmolarity changes through the changing in the volume of the
osmoreceptor (neurons will change APs)
o Located in and around the hypothalamus
o Increase in plasma osmolarity (decreased total body water) causes osmoreceptors
to physically decrease in volume, ADH released
High plasma osmolarity = water moves out of the cells by osmosis =
osmoreceptors cause body to release ADH
- When ADH is in the blood, it acts on the collecting duct of the nephron
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ADH action
- Increase water reabsorption in the collecting duct
- Collecting duct has aquaporin II water channels
o Aquaporin II channels can move in and out of the luminal membrane
- When ADH binds to receptor on basolateral membrane, there is a signal cascade that takes
water channels in vesicles and fuses them with the luminal membrane
- Trigger of ADH causes insertion of more aquaporin II water channels into the luminal
membrane
- More water channels = increase water absorption
- High ADH = ECF fluid is low = body wants to conserve water = maximize water reabsorb.
Decreased levels ADH levels in blood
- Decreased water reabsorption in the collecting duct
- Don’t have binding of receptors = vesicles endocytose the aquaprin )) channels
- Distinct situation: no aquaporin II on luminal membrane results in collecting duct cells
becoming impermeable to water
o = no motion of water
o None of the water in the filtrate as it is travelling through the collecting duct is
capable of being reabsorbed
- Unlike sodium pathway where 3 hormones can be released, ADH is the hormone that
balances water and is the only hormone that is released
o Either make more or less
o There is a gradient of ADH released in blood concentration will affect how much
water is reabsorbed
- ADH is a hormone that has a very short plasma life (couple minutes)
- To continue to do the job of reabsorbing more water, need constant ADH released in blood
o Higher conc. of ADH = more water reabsorbed by collecting duct
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Plasma osmolarity and ADH release
- Two major inputs control ADH and how much is released
- Plasma osmolarity can change a lot day to day
o E.g. average 70 kg individual - drink 1L of water = will change osmolarity by 7-8
mOsm (depending on mass)
o Larger you are, the more volume you have but can change volume quickly just by
drinking water
o Change in osmolarity is easily detectable
o Very small detectable changes: 1-2 mOsm
- Neuroendocrine cells can detect 1-2 mOsm differences and respond by releasing more or
less ADH
- Osmolarity is the MOST IMPORTANT FACTOR AND MOST SENSITIVE INPUT that
hypothalamic neurons will receive
- Osmolarity is detected by osmoreceptors (neurons found within and around the
hypothalamus)
o Osmoreceptors are located near the third ventricle near hypothalamus
o There are fenestrated capillaries in that ventricle that allow for quick changes in
interstitial fluid composition
o Although there is no blood in the brain, we have compartments that detect
osmolarity changes quickly (this is where osmoreceptors are located)
- Osmoreceptors respond to a change in osmolarity
- If osmolarity increases (less water, more solutes), osmoreceptors change the activity of
neuroendocrine cells
o Cell body of osmoreceptors shrivel in higher plasma osmolarity, leading to more APs
o Physical decrease in cell volume = osmoreceptors send more APs
o APs synapse on hypothalamic neurons that make ADH (but stored in posterior pit.)
o ADH is physically released from the posterior pituitary but cell body’s of neurons
are located in the hypothalamus)
- ADH goes through blood and travels through the kidney to increase water reabsorption
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