ADH effect on Na+

[cartman1980]

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Aldosterone is primarily responsible for Na+ absorption DCT and collecting ducts. It normally acts in conjunction w/ ADH to maintain plasma osmolarity.

If someone were to observe that Na+ re-absorption across epithelial cells of PCT and into peritubular capillary is significantly reduced then there is one definite possible cause of this (which i get):
- reduced glucose/amino acids concentration in blood

This is due to the functioning of secondary active SGLC or Na+-amino-acid cotransporters (which requires both materials being transported).

However, could the following not be a possible reason (i think it isn't but i can't spot the obvious flaw):

Reduced ADH secretion (due to whatever reason)-->lesser water reabsorption-->more loss of water in urine-->higher solute concentration-->higher osmolarity-->lesser Na+ gradient across the lumen of P/DCTs-->lesser Na+ being transported from apical into P/DCT (due to Na+-glucose/amino-acid/K-Cl cotransporter)-->lesser Na+ transported out from P/DCT into capillaries (via Na-K'ase pump)

I am sure i am incorrect; guess i just can't think straight anymore 🙂

Thanks

 

[Thirteeen]

Diabetes Insipidus caused by a deficiency in arginine vasopressin, aka ADH will cause such a problem. Patients tend to experience excessive urination and extreme thirst.

 

[Hah]

Aldosterone is primarily responsible for Na+ absorption DCT and collecting ducts. It normally acts in conjunction w/ ADH to maintain plasma osmolarity.

If someone were to observe that Na+ re-absorption across epithelial cells of PCT and into peritubular capillary is significantly reduced then there is one definite possible cause of this (which i get):
- reduced glucose/amino acids concentration in blood

This is due to the functioning of secondary active SGLC or Na+-amino-acid cotransporters (which requires both materials being transported).

However, could the following not be a possible reason (i think it isn't but i can't spot the obvious flaw):

Reduced ADH secretion (due to whatever reason)-->lesser water reabsorption-->more loss of water in urine-->higher solute concentration-->higher osmolarity-->lesser Na+ gradient across the lumen of P/DCTs-->lesser Na+ being transported from apical into P/DCT (due to Na+-glucose/amino-acid/K-Cl cotransporter)-->lesser Na+ transported out from P/DCT into capillaries (via Na-K'ase pump)

I am sure i am incorrect; guess i just can't think straight anymore 🙂

Thanks

Yea I think you are over thinking this. Sodium ALWAYS follows water so if water is going back into the body then sodium will follow the water to a certain point. If plasma osmolarity becomes far too high than mechanisms will occur to reduce it (reducing ADH and Aldosterone levels)

Bottom line is that reduced ADH will cause reduced Na+ reabsorption because less water is being reabsorbed.

I hope I am answering your question cause I'm not entirely sure what you were asking.

 

[cartman1980]

I hope I am answering your question cause I'm not entirely sure what you were asking.

The thought process stems from a question in TBR Bio-I. The question asked the most likely cause of reduced Na reabsorption across epithelial cells of PCT and into peritubular capillary. Options were
A,B: Irrelevant
C: reduced ADH secretion
D. reduced blood sugar concentration

So, i was trying to understand whether
a) /C/ is a valid scenario
b) if so, why /C/ is the better answer compared to /D/

 

[SmurfinUSA]

But make sure you clear ADH vs Aldosterone's mechanism of action.

ADH (vasopressin) is ALWAYS DIGGING HOLES via aquaporins in the collecting duct(from EK). just water moves

Aldosterone works on dist. conv. tub. to increase Na reabsorption, which leads to water following osmotic gradient.

 

[Hah]

The thought process stems from a question in TBR Bio-I. The question asked the most likely cause of reduced Na reabsorption across epithelial cells of PCT and into peritubular capillary. Options were
A,B: Irrelevant
C: reduced ADH secretion
D. reduced blood sugar concentration

So, i was trying to understand whether
a) /C/ is a valid scenario
b) if so, why /C/ is the better answer compared to /D/

I would think C is the correct answer. For the reasons I listed above. Why its better than D? I think it's because glucose concentration does not dictate Na reabsorption directly, it's merely a player in a few transport proteins. Na reabsorption is dependent on sodium plasma osmolarity and the body's state of hydration. Just think of what would happen if your body had a high sugar level and a high level of salt and dehydration. The high sugar level would not cause Na to be reabsorbed back. Rather, the ADH and Aldosterone levels (which will be low in this situation) will dictate the Na to be secreted.

 

[cartman1980]

I would think C is the correct answer.

This very confusion is the basis of my question. The answer is /D/. If blood glucose concentration is low, the SGLC co-transporter system will transport less of both Na+ and GLC (glucose) from apical to P/DCT because remember that for a cotransporter to work, all the materials it is transporting need to bind to the site. Roughly speaking, if there are 10 molecules of Na+, but only 2 molecules of glucose, the SGLC cotransport will only be able to transport 2 molecules of Na+ and 2 molecules of glucose across.

 

[Hah]

This very confusion is the basis of my question. The answer is /D/. If blood glucose concentration is low, the SGLC co-transporter system will transport less of both Na+ and GLC (glucose) from apical to P/DCT because remember that for a cotransporter to work, all the materials it is transporting need to bind to the site. Roughly speaking, if there are 10 molecules of Na+, but only 2 molecules of glucose, the SGLC cotransport will only be able to transport 2 molecules of Na+ and 2 molecules of glucose across.

Hmmm... then maybe it has to do with the regional specificity of the hormones?

ADH acts on the collecting tube and Aldosterone acts on the distal convoluted tubule.

The question does specifically refer to the PCT and not overall Na+ reabsorption so maybe the question is trying to teach you the importance of the nephron's regional specificity.

 

[flodhi1]

Yea I think you are over thinking this. Sodium ALWAYS follows water so if water is going back into the body then sodium will follow the water to a certain point. If plasma osmolarity becomes far too high than mechanisms will occur to reduce it (reducing ADH and Aldosterone levels)

Bottom line is that reduced ADH will cause reduced Na+ reabsorption because less water is being reabsorbed.

I hope I am answering your question cause I'm not entirely sure what you were asking.

Hmm? I think you got this upside down WATER FOLLOWS Sodium.

 

[flodhi1]

The thought process stems from a question in TBR Bio-I. The question asked the most likely cause of reduced Na reabsorption across epithelial cells of PCT and into peritubular capillary. Options were
A,B: Irrelevant
C: reduced ADH secretion
D. reduced blood sugar concentration

So, i was trying to understand whether
a) /C/ is a valid scenario
b) if so, why /C/ is the better answer compared to /D/

C is most definitely not the answer. The re absorption of water does NOT dictate the reabsorption of Sodium. Thus ADH (Vasopressin) plays NO ROLE in the reabsorption of Sodium.
For answer D my reasoning would have been that reduced blood sugar concentration means reduced solute in the blood. However it all depends on how much solute is present in the urine with respect to the blood. If there's MORE solute in the urine than you would have increased reabsorption. However if the amount of sodium (solute) is less than the amount of glucose (solute) in the blood you would NOT have reabsorption thus decreased reabsorption. By the way please for the love of GOD do not confuse Na+ reabsorption OR lack there of with ADH even if it's with respect to water reabsorption through the aquaporin channels.

 

[Hah]

Hmm? I think you got this upside down WATER FOLLOWS Sodium.

Oops, yes your right.