furosemide effects on nephron concentration

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ktrn305

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I would appreciate clarification on this concept. Blocking the NaClK symporter of the TAL with furosemide should directly decrease urine dilution while directly increasing urine concentration in the nephron.... correct? You are are preventing solute reabsorption and leaving more in the nephron than normal. However, considering the single effect mechanism, blocking NaClK would still decrease urine dilution, but this also decreases the CP osmotic gradient of the interstitium, which would decrease urine concentration by causing less H2O reabsorption along the descending limb. So furosemide definitely decreases urine dilution, but increases and decreases urine concentration in different contexts?

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furosemide inhibits the sodium-potassium-chloride cotransporter in the thick ascending limb. This transporter normally reabsorbs about 25% of the sodium load; therefore, inhibition of this pump can lead to a significant increase in the distal tubular concentration of sodium, reduced hypertonicity of the surrounding interstitium, and less water reabsorption in the collecting duct. This altered handling of sodium and water leads to both diuresis (increased water loss) and natriuresis (increased sodium loss). By acting on the thick ascending limb, which handles a significant fraction of sodium reabsorption, loop diuretics are very powerful diuretics. (CV Pharmacology | Diuretics)
 
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