Flashcards in sodium reabsorption Deck (20)
What determines the volume of the extracellular water compartment?
sodium as it is predominant cation in the ECF
Most of the Na reabsorption occurs in the early PCT. Two things make this possible, what are they?
Na/H exchange, powered by the Na/K ATPase pump and Na/glucose exchange, also powered by Na/K pump
In the late PCT, _______% of Na reabsorption is by passive transport
50% (The rest is Na/K pump)
Water in the ___________ is reabsorbed in a way that is isosmotic
True or False, Increased GRF (and FF) will alter the amount of sodium absorbed or secreted.
False! Increased filtration will result in increased oncotic pressure in the capillaries which will also increase sodium reabsorption proportionately (via solvent drag) to maintain constant 67% reabsorption.
Also, Increased GFR also means increased load of glucose and AA's are filtered, their reabsorption is couples with sodium. They will all be reabsorbed proportionally
What osmotically active agents are related to sodium reabsorption?
glucose and AA's
What hormonal factors stimulate sodium/water reabsorption at the pct?
AT2 and sympathetic NT's
What hormonal factors inhibit sodium/water reabsorption at the pct?
NO and BNP
What diuretics target the PCT? What complications will this involve?
Na/K ATPas inhibitors, carbonic anhydrase inhibitors (Diamox), osmotic diuretics (mannitol)
What is being filtered/absorbed in the PCT?
sodium is filtered!
What is being filtered/absorbed in the thin descending limb?
No sodium!!! H2O is being passively reabsorbed
What is being filtered/absorbed in the thin ascending limb?
Passive reabsorption of NaCl. NO water!!!
What is being filtered/absorbed in the thick ascending limb?
50/50 passive and active reabsorption of NaCl accounts for 25% of total Na reabsorption. NO water!!
In addition to AT2 and SNS, what other hormonal factors affect Na reabsorption in the thick ascending limb?
aldosterone and ADH
What is the active transport mediator in the thick ascending limb?
________ diuretics inhibit the Na/K/Cl symporter
What is happening with loop diuretics, how do they work?
the Na/K/Cl symporter is responsible for 50% of the 25% of Na reabsorption taking place in the nephron. So without this symporter there is about 12.5% more osmotically active Na in the nephron which pulls in a bunch of water to be wasted in the urine.
What else is reabsorbed by Na/K/Cl symporter that will be lost in the urine if not reabsorbed?
what is the potassium sparing diuretic? and How does it work
spironolactone, it binds to the mineralocorticoid receptor that typically receives aldosterone