Session 4- Volume control Flashcards
What does water in ECF most depend on
Na+
When we say Na reabsorption, what do we infer goes with it?
Cl-
Why can’t we just move water?
That would change osmolarity and we want to keep ECF isosmotic
If dehydrated how much water can be absorbed in CD?
25%
What is the target of aldosterone?
Acts in late DCT and CD principle cells
Specifically on ENaC and ROMK (increase Na in and increase K out)
If renal artery BP increases, how does that affect Na and H20?
PCT reabsorption goes down because NHE and NaKATPase function reduces. Plus its going faster through tubule so harder for things to move in.
Pressure natriuresis and pressure diuresis occur (more sodium and more water excreted)
Aquaporin location and type
AQP1 in PCT & DL
AQP7 in lower PCT
AQP 2,3,4 in CD
Three different segments of PCT and differences?
S1, S2, S3
S1 has SGLT2 (90% of glucose absorbed here)
S3 has SGLT1
What is bulk transport?
Reabsorption is isosmotic with plasma, water moves with solute
Water is only reabsorbed in which direction of tubule…
Descending
Like rain!!
What happens in LoH? Relate to structure
Descending is all permeable to water and impermeable to ions. passive water secretion, thin walls
Ascending is impermeable to water and permeable to solute. Lots of mitochondria and active transport
- So first descending lets water out (=its reabsorbed), then the filtrate arriving at ascending is more concentrated.
- So thin ascending lets ions leave into medulla (are reabsorbed) passively paracellulary
- Thick ascending NKCC so Na and K and Cl actively reabsorbed, ROMK puts K ions bacl
Which part of the nephron uses the most energy and is the most sensitive to hypoxia
Thick ascending limb of LoH
What is tubular fluid leaving nephron compared to plasma?
Hypo-osmotic
Water permeability of DCT is….
Fairly low
How is water permeability of late DCT and CD increased?
With ADH
Name transporters in early and late DCT
Early DCT: NCCT, ENaC
Late DCT: ENac
Describe omsolarity of tubular fluid before and after the DCT
As it arrives it is hypo-osmotic, leaves more hypo-osmotic (i.e. is more dilute)
DCT is a major site for ______ reabsorption
Calcium
Movement of Na through ENaC drives paracellular absorption of…
Cl-
Describe calcium reabsorption (and what it’s tightly regulated by)
Enters via TRPV5, shuttled to basolateral side by calbindin, transported out by NCX
Regulated by PTH
What are the two main cell types of the CD and what is their division of labour
Principle cells which reasborb Na via ENaC
Intercalated cells which reabsorb Cl-
Two types of IC cells?
Type A secretes H+, type B secretes HCO3
How is ADH controlled
Osmoreceptors in the OVLT of hypothalamus (also linked with nearby baroreceptors) detect low water. Signal to post pit to release ADH. Also signal to brain for thirst behaviour
What’s the only real way to control osmolality
Change water intake
By what % has osmolarity already changed if you’re thirsty
10%
Where does ADH act?
late DCT and CD on AQP2 in apical membrane
Causes of diabetes insipidus?
Central- doesn’t make enough ADH e.g. basilar skull fracture, meningitis, encephalitis, tumour, hypo/pit damage
Nephrogenic- kidney doesn’t respond to ADH
What is SIADH
Syndrome of Inappropriate ADH secretion, make too much
Sign of SIADH
Dilutional hyponatremia, oedema
Describe the cellular structure of the PCT
Brush border, lots of mitochondria, star shaped lumen
Compare and contrast SIADH and diabetes insipidus
Insipidus- not making ADH. All water not reabsorbed so polydipsia and hypovolemic and thirsty
SIADH- excessive ADH. Too much water reabsorbed so concentrated ursine but euvolemic because ANP causes natriuresis. Hyponatremic
Both can be caused by Head injury
Define hyponatremia
Less than 135mmol/L
Causes of hyponatremia
By far most common is too much water
True Na loss from d and v, renal failure, burns
