countercurrant mechanism

[aspiringmd1015]

---

Members don't see this ad.

the medullary osmolar gradient that is established is due to the nacl and urea, so it says if the PCT for whatever reason doesn't reabsorb its normal amount of water and electrolytes, this will overhwelm the loop of henle, which will then diminish the medullary interstitial osmolar gradient bc normally the loop of henle is responsible for establishing this gradient. How is this so?

 

[Jabbed]

It's essentially the same mechanism by which a massive water diuresis in primary polydipsia would wash out the medullary gradient: you have an abnormally large flux of water across the thin descending loop that dilutes the medullary interstitium.

 

[aspiringmd1015]

okay so poor osmotic gradient, so water can't be pulled out of the tubular fluid, so how does this effect ADH's affect to concentrate the urine? ADH already has a prerequisite to have a somewhat concentrated urine delivered to it? that can't be the case bc in the early distal tubule the fluid is hyposmolar(100)

 

[Jabbed]

okay so poor osmotic gradient, so water can't be pulled out of the tubular fluid, so how does this effect ADH's affect to concentrate the urine? ADH already has a prerequisite to have a somewhat concentrated urine delivered to it? that can't be the case bc in the early distal tubule the fluid is hyposmolar(100)

Remember that ADH doesn't actually pump water out of the collecting ducts, it inserts aquaporins that allow water to passively diffuse out of the collecting ducts into the interstitium. So if the concentration gradient of the interstitium decreases...

 

[IndiaInk567]

Jabbed is exactly right, but here's my way of thinking if it helps: Step 1: Excess water to descending loop (bcuz of prox tubule dysfunction). Step 2: Excess water resorbed into medulla in loop of henle --> medula becomes hypotonic. Step 3: Distal tubule resorbs less (despite ADH) because ADH opens channels but the gradient is diminished for resorption. Make sense?