I'm having a hard time understanding this.
It seems to me that from the TALH on to the collecting duct, sodium reabsorption and water reabsorption are unlinked. Sodium reabsorption is dependent on aldosterone. Water reabsorption is dependent on ADH and the fact that there's a massive osmotic gradient as you head down the medulla.
Why then would thiazides increase urine output? The only think I can think of is blockage of DCT sodium transporters means less sodium in the blood and a lower serum osmolarity. This would then cause greater supression of ADH which would lead to more urine output?
It seems to me that from the TALH on to the collecting duct, sodium reabsorption and water reabsorption are unlinked. Sodium reabsorption is dependent on aldosterone. Water reabsorption is dependent on ADH and the fact that there's a massive osmotic gradient as you head down the medulla.
Why then would thiazides increase urine output? The only think I can think of is blockage of DCT sodium transporters means less sodium in the blood and a lower serum osmolarity. This would then cause greater supression of ADH which would lead to more urine output?
