Osmolarity
Total solute concentration of a solution
The higher the osmolarity the lower the water content
Hypo-osmotic
Having a total osmolarity (solute concentration) of less the 300 mOsm (the normal extracellular fluid concentration)
Hyperosmotic
Having an osmolarity of more than 300 mOsm (that of normal extracellular fluid)
ISO-osmotic
Having the same osmolarity of the normal extracellular fluid, 300 mOsm
Where is water mainly reabsorbed
PCT, the majority of it, 99%
Where does water reabsorption regulation take place
In CD, specifically MCD
What does water reabsorption in the PCT depend on (details)
Depends on Na reabsorption
When Na is pumped back into the epithelial cells and peritubular capillaries, it decreases the osmolarity is the filtrate in the tubule (PCT in this case) and increases it in the interstitial fluid, giving up an osmotic gradient (high water in tubule vs low water in interstitium), on which water can flow down, effectively leaving the tubule and entering the interstitium to be reabsorbed by peritubular capillaries to even out the gradient and reach equilibrium (just like in diffusion)
How does water physically get from the tubule to the interstitium
Can flow paracellularly, diffusing between the epithelial cells, this is what happens in PCT
What 2 main factors does urine concentration depend on
The hyperosmolarity of the interstitial fluid (ability to pull water back in)
The presence fo vasopressin (hormonal regulation)
Countercurrent multiplier system (function not mechanism)
Countercurrent because flow goes in opposite directions (down, towards the medulla/loop of henle, in the thick descending limb, and then upwards after the loop of henle, in the thick ascending limb)
This system generates the hyperosmotic interstitial fluid
Mechanism of the countercurrent multiplier system
Filtrate leaves PCT, 99% has been absorbed, time for that 1%
Step 1:Once the filtrate gets to the thick ascending limb, lots of NaCl is reabsorbed, but not water, this region is impermeable to water, resulting in a hyperosmotic interstitium (slightly nothing crazy, like 400 mOsm)
Step 2: In the thick descending limb filtrate, no NaCl is reabsorbed, but water is pushed out in response to the hyperosmolarity of the interstitium (caused by step 1), making a hyperosmotic tubule filtrate that matches that of the interstitium (400 for both)
Step 3: the hyperosmotic filtrate flows from thick descending to ascending, the Na is reabsorbed into teh interstitium, increases hyperosmolarity, this forces the pulling of fluid from the thick descending limb and its cyclical, feeds each other
Vasa recta
Portion of peritubular capillaries that runs down into the medulla and then comes back up
How does the vasa recta prevent excessive solute loss from interstitium
Uses the same hairpin structure, loop, that basically has the same cyclical nature of the counterpart multiplier system
Can water pass by the DCT
No
Vasopressin (specs)
Peptide hormone produced by hypothalamus, aka ADH, released from posterior pituitary upon request though
Couples by GPCR to V1 (smooth muscle) and V2 (kidney)
Goal is the insertion of aquaporins into the luminal membrane of the CD cells to increase water permeability and retention
Diabetes insipidus
Caused by a malfunction in the vasopressin system, its not produced or there are no receptors such that theres no retention or reabsorption of water, it just all flows out, pale urine produced constantly
How does water reabsorption occur from DCT onwards (under influence of vasopressin)
No reabsorption in DCT but the filtrate is hypo-osmotic, interstitium hyper osmotic, so when we get to the CCD where it is permeable to water, water rushes out from the filtrate to equilibriate the two, getting them closer to iso-osmotic
As we descend down the MCD the interstitium becomes even more hyperosmotic (as it was the lower we got to the loop of henle), and consequently more water is reabsorbed
Water can pass at this time due to vasopressin opening/inserted aquaporins into the membrane
What regulates the release of vasopressin (details)
Osmoreceptor control (biggest factor): high fluid intake, more diluted plasma, osmolarity goes down, osmoreceptors in the hypothalamus detect this and sound the alarm, activity of them goes down, ADH is suppressed, water is let out, 1% change is enough to trigger
Baroreceptors control: senses more plasma volume, BP, high volume is indicative of increased fluid intake and results in ADH suppressor to bring it back down, Baroreceptor activity increases in this case, triggered by 3-5% change
Opposite is true for both
What factors cause thirst
High plasma osmolarity
Decreased plasma volume: if theres a big enough plasma drop and the RAAS is stimulated, angiotensin 2 will trigger thirst
Both signal the thirst region of the brain
Other minor ones include dry mouth and metering of water intake