Physiology 3120 Lecture Notes - Lecture 41: Posterior Pituitary, Osmoreceptor, Collecting Duct System
15 May 2018
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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
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Lecture 41 hormone regulation of water absorption. Regulation of water balance is through one hormone, ad( (cid:523)either make it or don"t(cid:524) The volume of the extracellular fluid (ecf) is linked to blood pressure: high fluid volume = increases blood pressure. 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: hypothalamus has neurons that project to and make the posterior pituitary, cell bodies of the neurons are located in the hypothalamus and they make adh. Vesicles with adh are stored in the posterior pituitary: adh is stored in the axon terminals of the nerves (location in posterior pit) Triggered for release by low ecf volume, high plasma osmolarity and angiotensin ii: not having enough body water = higher solutes. Integration between sodium and water balance with ang ii.
