Renal 4 Flashcards
Describe the thick ascending limb of NA reabsorption
Loop of henele: thick acending limb
Descending thin limb: sodium impermeable
Ascending thin limb: sodium permeable, some passive Na rebsorption
Thick ascending limb: TAL (s6) relies on NKC22 and sodium potassium pump for reabsorption
- It's thick because the cells are thick. Have mitochondira and have sodium potassium pumps in high activity. (diameter of fluid is the same, but cells get bigger) - Hypertonic interstitial and hypotonic tubular fluid that reenters cortex in DCT - K+ recycled to tubular lumen (required for NKCC activity) makes the lumen positive - Also sodium going out on basolateral side makes it more positive - Positive lumen makes cation reabsorbed.
NKCC2: moves sodium chloride and potassium. MAIN SODIUM REABSORPTION ACROSS EPITHELIAL CELLS ON APICAL SIDE.
- Dependent of availability of the 3 ions. (cl, k, na) there won't be a lot of potassium. - Use sodium gradient to move it across (down its gradient) which helps transport potassium into the cell too. - Then sodium carried out by active transport on basolateral side (sodium potassium pump) This activity is greater!
ROMK: Apical potassium channels:
- When potassium come in (from low to high) potassium leaves through these channels - Allows sodium to be recycled.
Describe distal tuble na reabsorption
DCT1
Early section of distal tuble: sodium potassium atpase + NCC (apical sodium chloride transporter)
DCT 2
NCC and sodium channel ENaC (epitheliam sodium channel)
- Down gradient, through channel across cell
- Electrogenic (not paired)
- Depending on activity of NCC or earlier region at EnaC: variable lumen potential (negative lumen potential here)
Thiazides and Amiloride: therapeuticially inhibit NCC or ENaC respectively. Alter sodium reabsorption, aleviate high blood pressure.
NCC: electroneutral
ENAc: electrogenic
Describe collecting duct na reabsorption
Collecting duct
- Principal cells rely on ENaC
- Site of regulation for na reabsorption (tuned by aldosterone)
Aldosterone enhances
- ENAC synthesis/production
- Apical insertion of ENAC (insert channels)
- Open probability of ENAC (channels more likely to be open, more able to reabsorb sodium)
Alter how much sodium is reabsorbed in collecting duct SPECIFICALLY.
Sodium enters through ENaC and exits with Sodium potassium ATPase
Summarize where transporters are and bulk flow of na reabsorption
Bulk Na occurs in PT
- NHE (proton exchanger)?? Sodium cotransporters
Minimal in thin loops of henle
Hypertonic interstitial is established by na reabsorption in TAL
- This region is important for moving sodium into interstital space that surrounds loop of henele.
- NKCC2, NCC, ENAC channels
Hormone regulation by aldosterone in the collecting duct.
Maximize sodium reabsorption
Summarize k+ reabsorption and secretion
This is super duper boring.
Sodium is ALWAYS reabsorbed, direction of transport is always the same.
Potassium goes in AND out. (absorption and secretrion)
- Dependent on amount of potassium in the plasma and whatever is delivered to the tuble in tubular fluid
Bulk K+ reabsortpions happens in proximal tubule
- PT and TAL is same for all potassium levels - Same for sodium and water (67% at PT + 20% at TAL)
Regulation of K+
Reabsorption/secretion occurs in the collecting ducts (and some distal tubule)
- Normal or elevated K= secretion predominates (net 15-80% at the end)
- Low K+ levels: reabsoprtion predominates. (reabsorption CONTINUES, net 1%)
what are the two major pathways of proximal tubule K+ reabsorption
Two major pathways:
- Solvent drag K+ reabsorption (early PT, negative)
○ Active NA reabsorption drives H20 reabsorption and the bulk h20 movement is coupled with K+ movement
- Paracellular diffusion (later PT, positive)
○ Positive tubular lumen drives this reabsorption.
○ More reliant on diffusion
The tubular lumen potential are being compared to the peritubular space. Inside of cell is negative compared to both of these regions.
Describe how transport altersn tubular fluid composition and decreases flow rate? (how does fluid change in the tubule as you move along the PT)
- Inulin is freely filtered at glomerulus and is not reabsorbed/secreted. Inulin is constant, can be used for comparisions.
TF/P: concentration of solute in tubular fluid to solute in plasma at a given distance along the tubule.
Lack of protein in tubular fluid
Variable amount of reabsoption of substances along the tubule (sodium, potassium, chloride, bicarbonate, amino acids)
- Bicarb/amino acids happen rapidly and strongly
1. Fluid changes across the tubule - Glucose, AA and bicarbonate are reabsorbed - H20 is reduced (only know this because of inulin is constant, but concentration changes!) - H20 follows na movement (because of osmolality ) ○ Fluid starts by resembling plasma (without proteins) and then basically becomes NaCl 2. Transepitheial potential (PD) is negative but becomes positive. Gives positive lumen potential (transcelluar stuff). Changes won't always be the same. 3. Tubular fluid flow decreases progressively along PT (because you're absorbing H20 ) (leaky hose analogy, since you're losing water already there will be less flow)
Describe the distal convoluted tubule K+ secretion
KCC is APICAL this time (last segment it was on the basolateral side, helping with reabosption)
= allows you to direct it towards secretion (into the lumen/to be excreted)
- Major pathway in DCT
- Late DCT secrettion of K relies on KCC and ROMK
○ Romk in DCT mediates a major K+ secretory pathway
Describe the collecting duct region of K+ secretion/absorption
See all the types of channel’s that we’ve discussed.
Principle cells of collecting duct.
Transport relieant on KCC and exit through ROMK
- For secreting potassium in normal or elevated state.
- Results in increased potassium excreteion. (15-80% comes from here)
- MaxiK has low activity in normal situations. But high tubular flow, the maxiK is flow dependent: so then maxiK will contribute to secertion of potassium
Increased tubular flow: K+ secreted more and mediated by MaxiK
