Aldosterone's effect on plasma tonicity

[BlondeCookie]

One of aldosterone's primary effects is the resorption of Na+ from the kidney's. Na+ is reabsorbed and then water follows. Is the solution is resorbed from the kidneys to the ECF and isotonic or hypertonic solution?

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[Ms MD]

i think it's isotonic, because water follows, as you said.

 

[physics junkie]

isotonic.

 

[BlondeCookie]

If aldosterone allows for the resorption of an isotonic solution from the kidneys, how would that explain for hyperaldosteronism? If I am not mistaken, hyperaldosteronism allows for the resorption of a hypertonic solution from the kidneys to the ECF. This explains the hypernatremia a patient with hyperaldonsteronism has.

 

[physics junkie]

I wish I could put to words my frustration that my long, drawn out post didn't show up when I posted it yesterday.

Here are the cliff notes:

Aldosterone increases Na+ reabsorption and K+ secretion. The hypernatremia is not a result of a change in plasma tonicity. What actually happens is that the Na+ reabsorption causes osmolality receptors to send signals to release ADH(the real hormone in charge of osmoregulation) and this allows water to follow the reabsorbed Na+ passively out of the collecting duct in to the plasma.

 

[eduro25]

Hey physics , nice explanation , can you give us the source please,
Thanks in advance.
Regards,
Eduro

 

[BlondeCookie]

I wish I could put to words my frustration that my long, drawn out post didn't show up when I posted it yesterday.

Here are the cliff notes:

Aldosterone increases Na+ reabsorption and K+ secretion. The hypernatremia is not a result of a change in plasma tonicity. What actually happens is that the Na+ reabsorption causes osmolality receptors to send signals to release ADH(the real hormone in charge of osmoregulation) and this allows water to follow the reabsorbed Na+ passively out of the collecting duct in to the plasma.

Can someone please clarify this a bit more? What I am understanding is this... Hypernatremia results as a result of hyperaldosteronism. Thus, a hypertonic solution must have entered the ECF's vascular space to give that hypernatremia.... so, wouldn't it make sense that aldosterone caused a hypertonic absorption of fluid from the kidneys?

Maybe I am missing something here because already two people on this thread have said that aldosterone reabsorbs an isotonic rather than a hypertonic solution.

 

[FutureDoc4]

I'll bite:

Blonde Cookie, you are thinking about this in the wrong way.

Aldosterone acts on the prinicpal cells in the late distal tubule (and somewhat the collecting duct).

Ignore, H20 for a sec. Aldosterone causes an increase in sodium reabsorbtion and K+ secretion.

This increase in sodium, increases the osmolarity of the plamsa, sensed by osmalality receptors in the hypothalamus, which signal the posterior pituitary to release ADH.

ADH acts on the Prinicipal cells in the late distal tubule and collecting duct to increase water permeability. The increased water permeability will cause water to flow and equilibrate returning the plasma osmalarity to normal, giving the "appereance" that water simply followed Na+ sodium directly into the plasma (an isotonic fluid as some indicated).

However, in the absence of ADH the principal cells are virtually impermeable to water. So, it is not as simple as water following sodium or the absorbtion of an isotonic or hypertonic solution.

BRS Physio pg. 166.

In regards to hyperaldosteronism, I would guess, that ADH release and water reabsorbtion cannot keep up with the increase Na+ reabsortion (giving you hypernatremia).

 

[str8flexed]

Great explanation by the above post. I agree that the body may be "one step behind" with ADH's action of water absorption so your blood will be slightly hypertonic.

 

[physics junkie]

Everything FutureDoc04 is correct but I'll reply anyways.

Let's go over osmolarity real quick first. Osmolarity is the concentration of particles in a solution expressed in this equation: Osmolarity = # of solutes / liters of pure water.

In our case our 'solution' is extracellular fluid which is made up of blood and interstitial fluid.

You can increase osmolarity in two ways:
1) you can decrease the amount of pure water in the solution
2) you can increase the # of solutes. This is how aldosterone works.
3) add a fluid that is hypertonic to blood to the blood...but this is just the same as adding a lot of solutes and a little bit of water so its redundant for #1 and #2.

You can decrease the osmolarity of a solution in two ways:
1) you can increase the amount of pure water in the solution. This is how ADH works.
2) you can decrease the # of solutes.

Remember, Na+ is the highest concentration electrolyte in the extracellular space and thus the main regulator of water balance. On the other hand, the concentration of K+ in the extracellular fluid is very low all the time(in fact the K+ that is secreted by the kidney has to first diffuse out of the cytoplasm of cells throughout the body to go to the kidney to be secreted). K+ is high in concentration in the intracellular fluid but this doesn't really play a role in the water balance of the cell since there are so many proteins and other solutes in the cell that contribute to the osmolarity of the intracellular space.

When the osmoreceptors in the extracellular space sense that the blood is hypertonic compared to its usual state they stimulate the hypothalamus to release ADH. ADH puts aquaporin2 channels into the late distal tubule & collecting duct. Aquaporin2 channels will only allow pure H2O to be reabsorbed.(Wiki says: Aquaporins selectively conduct water molecules in and out of the cell, while preventing the passage of ions and other solutes.)

With ADH present the water from the ultrafiltrate will flow passively through aquaporin2 channel through the principal cells to the blood. This will bring the osmolarity of the blood down(and raise the osmolarity of the urine). If water can't diffuse from the ultrafiltrate to the blood fast enough to bring down the osmolarity of the blood then osmolarity receptors will signal for more and more ADH release.

To recap:

1) Aldosterone makes the blood hypertonic by adding Na+.
2) Osmolarity receptors signal ADH release to place aquaporin2 channels in the late DCT/collecting duct. This allow the absorption of pure water from the ultrafiltrate(pure water is hypotonic to blood).
3) The end result is that you get the equivalent of isotonic fluid reabsorption because osmoreceptors keep osmolarity tightly regulated and will release more ADH as necessary to keep blood osmolarity at normal physiological levels.

 

[Captopril]

I have too much ADD to read the lengthy explanations. Just wanted to throw this out there:

Don't forget about aldosterone escape cuz of ANP, etc.

 

[BlondeCookie]

Thank you all for the well-written help, especially Physics. I have a very good understanding of it now, but my original question is a little bit murky still.

True of false: aldosteronism results in hyperaldosteronism.

True or false: aldosterone only resorbs Na+, no water follows via osmosis

 

[physics junkie]

Thank you all for the well-written help, especially Physics. I have a very good understanding of it now, but my original question is a little bit murky still.

True of false: aldosteronism results in hyperaldosteronism.

A lot of aldosterone would give you hyperaldosteronism so yes.

True or false: aldosterone only resorbs Na+, no water follows via osmosis

true.

For your original question: the final result is that when the aldosterone is released the fluid reabsorbed from the kidney is isotonic to blood.

 

[Perudoc]

since this is a physio topic I have a question.
I have BRS physio second edition..is the third edition better? maybe more graphics?
Thanks

 

[hateroftheyear]

since this is a physio topic I have a question.
I have BRS physio second edition..is the third edition better? maybe more graphics?
Thanks

BRS physio didn't change much between editions. Don't worry about it. And don't focus too much on the finer details of Neurophysiology either, that section is overkill for the boards.