Case 7 Hot and thirsty

6 important questions on Case 7 Hot and thirsty

Reabsorption in early proximal convoluted tubule

Glucose, AA, phosphate, lactate, citrate. With sodium co-transporters, but sodium cannot build up inside the epithelial cells of the wall. So sodium/potassium ATPase and sodium/proton exchanger are used.

Reabsorption in the late proximal convoluted tubule

Fluid that enters lacks essential substances.
Reabsorption of Cl ions, highly concentrated due to the water reabsorption.
- Chloride anion exchanges (driven by high conc. of Cl)
- Passive movement through thigh junctions.
Sodium continues to be reabsorbed.

Reabsorption in thick ascending limb

further 25% of sodium and potassium is reabsorbed via
- Three-ion cotransporter (sodium/potassium/chloride)
- Sodium/potassium ATPase.
Sodium is actively pumped out, potassium and chloride diffuse down electrochemical gradient
No reabsorbing of water
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Reabsorption in distal tubule and collecting duct

These parts determine how much sodium will be excreted
There is a sodium/potassium ATPase
Also hormones which regulate the sodium reabsorption

Insensible water loss

Water loss we are not aware of (exhale for example)

Influence of ADH on water balance

Low ADH -> most water reaching the collecting duct can not be reabsorbed because the lack of aquaporins -> diluted urine and reduced volume of body fluids
High ADH -> Aquaporins are inserted in apical membranes -> nearly all the water is reabsorbed.
Osmoreceptors in hypothalamus sense ECF solute concentration and trigger/inhibit ADH release form the posterior pituitary.

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