question with kidney function (loop of henle)

[yoyohomieg5432]

I thought the point of the loop of henle was to concentrate the filtrate. this is because Na/Cl are pumped out and water follows. so the concentration of other solutes increases.

this picture from my A&P textbook is confusing me though. at the bottom of the loop it shows the filtrate is highly concentrated, which makes sense. however as it goes back up the ascending portion the concentration falls, eventually to even lower than when it first entered the loop (100 vs 300). the way im looking at this picture it seems like the loop isn't really concentrating? i don't understand

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[milski]

The increased concentration is in the medula itself. By controlling the permeability of the collecting duct you can control how much water flows into the medula and as a result how concentrated is the urine.

 

[Synapsis]

I thought the point of the loop of henle was to concentrate the filtrate. this is because Na/Cl are pumped out and water follows. so the concentration of other solutes increases.

this picture from my A&P textbook is confusing me though. at the bottom of the loop it shows the filtrate is highly concentrated, which makes sense. however as it goes back up the ascending portion the concentration falls, eventually to even lower than when it first entered the loop (100 vs 300). the way im looking at this picture it seems like the loop isn't really concentrating? i don't understand

I have a sequence that should help.

Going down the descending loop, there is water permability allowing reabsorption of water such that when the filtrate reaches the bottom of the loop, it's concentrated (decreasing water concentration increases osmolarity).

Going up the ascending loop, there's essentially no water permeability, but there are a lot of ion channels, including the Na,K, 2Cl symporter, which reabsorb ions, lowering osmolarity and decreasing concentration.

Then entering the collecting duct, concentration is changed again by AQP4 channels (under control of vasopressin/ADH) in the lumen. More vasopressin causes more reabsorption of water, leading to more concentrated urine.

Does this help?

 

[yoyohomieg5432]

I have a sequence that should help.

Going down the descending loop, there is water permability allowing reabsorption of water such that when the filtrate reaches the bottom of the loop, it's concentrated (decreasing water concentration increases osmolarity).

Going up the ascending loop, there's essentially no water permeability, but there are a lot of ion channels, including the Na,K, 2Cl symporter, which reabsorb ions, lowering osmolarity and decreasing concentration.

Then entering the collecting duct, concentration is changed again by AQP4 channels (under control of vasopressin/ADH) in the lumen. More vasopressin causes more reabsorption of water, leading to more concentrated urine.

Does this help?

makes sense. but i thought ADH/ aldosterone worked on the distal convoluting tubule? Does it also have the same effects on the collecting duct?

 

[Synapsis]

makes sense. but i thought ADH/ aldosterone worked on the distal convoluting tubule? Does it also have the same effects on the collecting duct?

ADH (I usually call it vasopressin because that's the first name I learned) is a peptide hormone that binds to V2R (Vasopressin2 Recepters) in basolateral membranes of kidney collecting duct cells. Since V2R is a GPCR, you get the "generic" signal transduction events of increase in Gs activity and increase in cAMP, which helps vesicles with AQP4 exocytose into the luminal membrane, where they allow reabsorption with water. People with Diabetes Insipidus usually have some defect in this pathway, which causes them to produce more urine (because they don't reabsorb as much water, it's expelled in urine). For example, they can have a mutation in the V2R receptor so that ADH isn't recognized, and AQP4 is never exocytosed.

I think that's way more detail than the MCAT cares, but yep, ADH works on collecting duct cells. I don't know that it works on the distal tubule (can someone check me?), and I know aldosterone works on both, and it increases Na reabsorption. But those two are definitely different.

Hope this helps some!

 

[yoyohomieg5432]

ADH (I usually call it vasopressin because that's the first name I learned) is a peptide hormone that binds to V2R (Vasopressin2 Recepters) in basolateral membranes of kidney collecting duct cells. Since V2R is a GPCR, you get the "generic" signal transduction events of increase in Gs activity and increase in cAMP, which helps vesicles with AQP4 exocytose into the luminal membrane, where they allow reabsorption with water. People with Diabetes Insipidus usually have some defect in this pathway, which causes them to produce more urine (because they don't reabsorb as much water, it's expelled in urine). For example, they can have a mutation in the V2R receptor so that ADH isn't recognized, and AQP4 is never exocytosed.

I think that's way more detail than the MCAT cares, but yep, ADH works on collecting duct cells. I don't know that it works on the distal tubule (can someone check me?), and I know aldosterone works on both, and it increases Na reabsorption. But those two are definitely different.

Hope this helps some!

i checked my A&P book again and it says that ADH does function on the DCT, but also on the collecting duct. so i guess ADH/aldosterone work on both

 

[deleted393595]

I thought the point of the loop of henle was to concentrate the filtrate. this is because Na/Cl are pumped out and water follows. so the concentration of other solutes increases.

this picture from my A&P textbook is confusing me though. at the bottom of the loop it shows the filtrate is highly concentrated, which makes sense. however as it goes back up the ascending portion the concentration falls, eventually to even lower than when it first entered the loop (100 vs 300). the way im looking at this picture it seems like the loop isn't really concentrating? i don't understand

Also, to add on to what the others have said, the purpose of the Loop of Henle is basically to generate an osmolarity gradient within the cortex to the medulla, and to send back up dilute filterate that the collecting duct can decide to concentrate or not concentrate (ADH acts here - for controlling ECF volume and osmolarity)

ADH (I usually call it vasopressin because that's the first name I learned) is a peptide hormone that binds to V2R (Vasopressin2 Recepters) in basolateral membranes of kidney collecting duct cells. Since V2R is a GPCR, you get the "generic" signal transduction events of increase in Gs activity and increase in cAMP, which helps vesicles with AQP4 exocytose into the luminal membrane, where they allow reabsorption with water. People with Diabetes Insipidus usually have some defect in this pathway, which causes them to produce more urine (because they don't reabsorb as much water, it's expelled in urine). For example, they can have a mutation in the V2R receptor so that ADH isn't recognized, and AQP4 is never exocytosed.

I think that's way more detail than the MCAT cares, but yep, ADH works on collecting duct cells. I don't know that it works on the distal tubule (can someone check me?), and I know aldosterone works on both, and it increases Na reabsorption. But those two are definitely different.

Hope this helps some!

Me thinks it's also APQ3 on the lumial membrane, but I don't have my physio textbook on me atm so I can't look it up