Renal Lecture 2 Flashcards
Where is most NaCl reabsorbed?
2/3 reabsorbed in the proximal tubule
Substances are reabsorbed across what?
renal tubular epithelial cells
Transcellular reabsorption vs paracellular reabsorption
transcellular (what mostly happens): through cells; active: at least one step is against concentration or electrochemical gradient
paracellular: between cells; passive: driven by concentration or electrochemical gradient
Na absorption in the early proximal tubule
On the apical side (urine) of the epithelial cell, many transporters actively accumulate many substances from the urine => gradient favours them to exit on the basolateral side and into the blood
SGLT transports Na and glucose into the cell, NHE = Na and H exchanger (Na in, H out)
On the basolateral side, Na is pumped out through an Na pump (Na,K-ATPase)
all transporters are only located on one membrane!!
Active glucose reabsorption in the proximal tubule
glucose in transported INTO the cell on the apical cell by SGLT (secondary active)
glucose is then passively transported OUT on the basolateral side by GLUT
Why does [Cl] go up in the proximal tubule instead of going down?
very little Cl is reabsorbed here, but the volume decreases (water is reabsorbed) causing the concentration to go up
Why is Na reabsorbed isosmotically in the proximal tubule?
because the same amount (2/3) of water is also reabsorbed in the proximal tubule
How do the Starling Forces favour fluid reabsorption?
while the hydrostatic pressure in the pretubular capillaries is higher than in the interstitial fluid (and therefore fluid SHOULD move to the fluid), the oncotic pressure is much higher in the capillary than in the fluid => more protein in capillaries draws more water and solutes in to lower this protein concentration
Na absorption in the late proximal tubule
- reabsorbed as NaCl
- active (transcellular) and passive (paracellular) components
- active transport is done by the Na,K-ATPase (K in, Na out)
- Na taken into cell from urine through NHE transporter
- Cl- brought in and leaves passively(?) (into blood)
- paracellular Na transport driven by transepithelial [Cl-] gradient
Na absorption in the ascending limb of the loop of henle
- reabsorbed in the form of NaCl
- NKCC brings in Na, 2Cl, and K from urine
- Na,K-ATPase on blood side to take Na out
- Cl and K leave on basolateral membrane
- absorbed WITHOUT water => this part of nephron is impermeable to water
furosemide: “loop” diuretic (targets NKCC - blocks Cl intake)
Na reabsorption in early distal tubule
- reabsorbed as NaCl, without water (still impermeable)
- NCC on lumen side: Na, Cl co-transporter
- thiazide diuretic blocks Cl intake on lumen side
- Cl leaves on basolateral side
- Na leaves through Na,K-ATPase
Na absorption in the late distal tubule and collecting duct
- ENaC brings in Na from lumen side
- Na,K-ATPase takes Na out on basolateral side and brings K in
- K is secreted into urine passively
- K-sparing diuretic: decreases Na reabsorption and K secretion
How do the kidneys balance sodium levels, and how does Na control extracellular fluid volume?
- the kidneys must match Na excretion to Na intake => if we suddenly increase our Na intake, our kidneys quickly catch up to match this with more excretion (and vice versa for decreased intake)
- if we increase our intake, our extracellular fluid volume increases, increasing blood pressure
What’s the relationship between sodium intake, ECF volume, and BP?
increase Na => increase ECF => increase BP => end result is more Na excretion
decrease Na => decrease ECF => decrease BP => end result is less Na excretion
How do the sympathetic nerves control Na excretion?
- by changing the afferent arteriolar resistance (and consequently GFR)
- decreased ECF volume leads to increased symp. activity, which causes increased resistance in the afferent arteriole
- leads to a decrease in GFR and ultimately decreased Na excretion
reverse happens if ECF volume goes up
Oncotic pressure in the control of Na excretion
increased ECF volume:
- decreases oncotic pressure and increases hydrostatic pressure
- decreases isotonic reabsorption
- increases Na secretion
decreased ECF volume:
- increased oncotic pressure and decreased hydrostatic pressure
- isotonic reabsorption increases
- Na excretion decreases
