Urea in the Corticomedulary Gradient

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StilgarMD

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After doing the BRS Cell Phys chapter, a peculiar question comes up about a 300 mM solution of Urea into the blood of a patient leading to massive RBC lysis. I understand a hypotonic solution will lead to water rushing into RBCs and leading to their bursting, but earlier in the chapter it is stated

"If the reflection coefficient is zero, the solute is completely permeable. Therefore, it
will not exert any osmotic effect, and it will not cause water flow. Urea (a small solute)
usually has a reflection coefficient of close to zero and it is, therefore, an ineffective
osmole."

This also is confusing in the context of what is stated in the kidney chapter:
"■   ADH stimulates a facilitated diffusion transporter for urea (UT1) in the inner medullary collecting
ducts. Urea reabsorption from inner medullary collecting ducts contributes to urea
recycling in the inner medulla and to the addition of urea to the corticopapillary osmotic
gradient."

So how does a molecule which is too small and hydrophobic to be stopped by a plasma membrane still exert enough of an osmotic gradient to help the kidney concentrate solute (and make RBCs explode despite being injected @ an Isotonic concentration)?
 
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