Aldosterone and Osmolarity

[G1SG2]

In TPR Bio, it says:

"When the BP is high, aldosterone is not released. As a result, sodium is lost in the urine. Plasma osmolarity (and eventually BP) fall. Other triggers for the release of aldosterone are low blood osmolarity, and low blood volume, and angiotensin II."

Okay, so basically what this means is that the plasma osmolarity falls when aldosterone is not released and sodium is lost in the urine...but if it falls too low, then that will trigger the release of aldosterone? Which increases the osmolarity by increasing the reabsorption of sodium, right (along with water, of course)?

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[matth87]

In TPR Bio, it says:

"When the BP is high, aldosterone is not released. As a result, sodium is lost in the urine. Plasma osmolarity (and eventually BP) fall. Other triggers for the release of aldosterone are low blood osmolarity, and low blood volume, and angiotensin II."

Okay, so basically what this means is that the plasma osmolarity falls when aldosterone is not released and sodium is lost in the urine...but if it falls too low, then that will trigger the release of aldosterone? Which increases the osmolarity by increasing the reabsorption of sodium, right (along with water, of course)?

Right aldosterone and ADH are released and worked together in order to increase blood osmolarity and then increase blood volume which will in turn increase blood pressure.

First Adolsterone increase osmolarity.
Then
ADH makes the DCT / collecting duct permeable to water and since the medulla is high osmolarity it will suck the water out and then the vasa recta will uptake the water right away.

Keep reading in the book they have a really nice example of the baroreceptor cells called JG and Macula Densa cells and a nice diagram of how those cells and renin and ADH, adolsterone, and angiotension all work in tandom to manipulate osmolarity, vasoconstriction, and plasma volume to change your blood pressure.

 

[muhali3]

I wouldn't say a lack of aldosterone directly decreases plasma osmolarity and BP. Aldosterone secretion is primarily stimulated by high K+ levels in relation to Na+ in the plasma. You're correct though that aldosterone restores plasma osmolarity and BP through an Na+/H20 symport channel.

 

[Charles_Carmichael]

In TPR Bio, it says:

"When the BP is high, aldosterone is not released. As a result, sodium is lost in the urine. Plasma osmolarity (and eventually BP) fall. Other triggers for the release of aldosterone are low blood osmolarity, and low blood volume, and angiotensin II."

Okay, so basically what this means is that the plasma osmolarity falls when aldosterone is not released and sodium is lost in the urine...but if it falls too low, then that will trigger the release of aldosterone? Which increases the osmolarity by increasing the reabsorption of sodium, right (along with water, of course)?

The way I think about it, ADH secretion is primarily regulated by osmolarity. There are osmoreceptors in the hypothalamus that detect plasma osmolarity; if osmolarity increases, ADH secretion is stimulated (and you also become thirsty) so that you can reabsorb water to restore osmolarity.

I think of aldosterone more in the sense of body fluid volumes and systemic pressure. If you are hypotensive, the renin-angiotensin-aldosterone system (RAAS) is activated due to a decrease in GFR. This decrease in GFR stimulates renin secretion which ultimately leads to aldosterone secretion and Na+ reabsorption and thus, increases body fluid volume and pressure.

So, in my view, ADH is more involved with regulating plasma osmolarity while aldosterone is more involved with maining systemic pressure (by regulating body fluid volume). I haven't encountered any practice questions that challenged the way I think about these two hormones (yet) so this line of thinking has been working pretty well for me. Hope this helps.

 

[Will Hunting]

The way I think about it, ADH secretion is primarily regulated by osmolarity. There are osmoreceptors in the hypothalamus that detect plasma osmolarity; if osmolarity increases, ADH secretion is stimulated (and you also become thirsty) so that you can reabsorb water to restore osmolarity.

I think of aldosterone more in the sense of body fluid volumes and systemic pressure. If you are hypotensive, the renin-angiotensin-aldosterone system (RAAS) is activated due to a decrease in GFR. This decrease in GFR stimulates renin secretion which ultimately leads to aldosterone secretion and Na+ reabsorption and thus, increases body fluid volume and pressure.

So, in my view, ADH is more involved with regulating plasma osmolarity while aldosterone is more involved with maining systemic pressure (by regulating body fluid volume). I haven't encountered any practice questions that challenged the way I think about these two hormones (yet) so this line of thinking has been working pretty well for me. Hope this helps.

You nailed it. In Campbell they specify that ADH is with osmolarity. If you eat salty foods you increase your osmolarity so this causes you to secrete ADH to decrease and makes you thirsty as Kaushik said. Don't think of ADH as blood pressure regulation, that is the purpose of renin as kaushik stated. Example, if you are in an accident and lose lots of blood. Your blood pressure is low but osmolarity is the same. ADH and aldosterone wouldn't respond to this. However, renin will and then will secondary activate ADH afterwords.

 

[G1SG2]

From my understanding, ACTH primarily stimulates the release of glucocorticoids, but it also sometimes stimulates the release of mineralocorticoids like aldosterone. In a discrete question in the TPR science workbook, I got a question wrong regarding aldosterone release from the pituitary gland. The explanation says "in reponse to low BP, angiotensin II stimulates aldosterone release from the adrenal cortex, not the pituitary gland". So, are we to assume that ACTH plays absolutely NO role in the release of aldosterone, and that aldosterone is solely regulated by the renin-angiotensin system?

 

[matth87]

From my understanding, ACTH primarily stimulates the release of glucocorticoids, but it also sometimes stimulates the release of mineralocorticoids like aldosterone. In a discrete question in the TPR science workbook, I got a question wrong regarding aldosterone release from the pituitary gland. The explanation says "in reponse to low BP, angiotensin II stimulates aldosterone release from the adrenal cortex, not the pituitary gland". So, are we to assume that ACTH plays absolutely NO role in the release of aldosterone, and that aldosterone is solely regulated by the renin-angiotensin system?

Tisk tisk you shouldn't be up studying at 4:00am! Haha, I was up till 4am last night to by the way. Don't know how im up at 7:00am right but anyways.

Adrenal Gland
Cortex - Aldosterone, Cotisole, Sex Steroids
Medulla - Ephinephrine

Anything dealing with blood pressure is just going to be Aldosterone related, but aldosterone is released from the adrenal cortex, not the pituitary gland.

Anything dealing with energy mobilization, glycogen break down, gluconeogensis (which entails some glycogen formation in the liver), stress (similar to "fear), sympathetic activation, is going to be ACTH and cortisol related.

This is an example of how having "to much information" can make you think to hard and get a question wrong.

 

[G1SG2]

Tisk tisk you shouldn't be up studying at 4:00am! Haha, I was up till 4am last night to by the way. Don't know how im up at 7:00am right but anyways.

Adrenal Gland
Cortex - Aldosterone, Cotisole, Sex Steroids
Medulla - Ephinephrine

Anything dealing with blood pressure is just going to be Aldosterone related, but aldosterone is released from the adrenal cortex, not the pituitary gland.

Anything dealing with energy mobilization, glycogen break down, gluconeogensis (which entails some glycogen formation in the liver), stress (similar to "fear), sympathetic activation, is going to be ACTH and cortisol related.

This is an example of how having "to much information" can make you think to hard and get a question wrong.

Oh okay, so basically the question implied aldosterone being directly released from the pituitary (without being mediated by ACTH)? Dammit, you're right, no more studying at 4 am, lol.

 

[matth87]

yo pookie I just picked up all the exam krackers books, how do you think they compare to the TPR books.

I have pretty much read each chapter close to 2 times now in the TPR. I read through a little bit of the EK stuff and they present it in a diff manner. Kinda cool studying from two different sources. I think its gonna help me remember stuff better.

 

[G1SG2]

yo pookie I just picked up all the exam krackers books, how do you think they compare to the TPR books.

I have pretty much read each chapter close to 2 times now in the TPR. I read through a little bit of the EK stuff and they present it in a diff manner. Kinda cool studying from two different sources. I think its gonna help me remember stuff better.

I think they'll be a breeze, especially since you've thoroughly read through the TPR stuff. But yeah, it's good to do content review from two different sources (I actually first started out with EK), and they certainly have some good mnemonics/way of presenting things.

 

[matth87]

I think they'll be a breeze, especially since you've thoroughly read through the TPR stuff. But yeah, it's good to do content review from two different sources (I actually first started out with EK), and they certainly have some good mnemonics/way of presenting things.

ADH always digging holes, I read this last night at like 3:00am, I think i laughed for like 10 minutes being so delirious

 

[G1SG2]

Just wanted to clear up something-can aldosterone in the renin-angiotensin system cause water reabsorption without ADH? I know it increases Na+ absorption, but does that automatically cause reabsorption of water because of increasing osmolarity, or does secondarily activated ADH need to help out?

 

[Charles_Carmichael]

Just wanted to clear up something-can aldosterone in the renin-angiotensin system cause water reabsorption without ADH? I know it increases Na+ absorption, but does that automatically cause reabsorption of water because of increasing osmolarity, or does secondarily activated ADH need to help out?

The early distal tubule is impermeable to water, just like the thick ascending LoH. Water absorption in the late distal tubule is variable. In the absence of ADH, there's very little water permeability of the principal cells (which are located in the late distal tubule); the water permeability of these principal cells is regulated by ADH.

 

[G1SG2]

The early distal tubule is impermeable to water, just like the thick ascending LoH. Water absorption in the late distal tubule is variable. In the absence of ADH, there's very little water permeability of the principal cells (which are located in the late distal tubule); the water permeability of these principal cells is regulated by ADH.

Gotchya, thanks.

 

[thebillsfan]

I think aldosterone can work without ADH. If youre creating a concentration gradient, water can still diffuse without the help of ADH. Of course, ADH will make things so much more efficient, but to say aldosterone NEEDS ADH to perform its function is a stretch

 

[Charles_Carmichael]

I think aldosterone can work without ADH. If youre creating a concentration gradient, water can still diffuse without the help of ADH. Of course, ADH will make things so much more efficient, but to say aldosterone NEEDS ADH to perform its function is a stretch

I don't think aldosterone can really function without ADH. The distal tubule has a "tight" epithelium, which would mean that the paracellular pathway (movement between cells; ie. not going through the cell but around it) is pretty much non-existent. An example of a "leaky" epithelium (where solutes and water can travel paracellularly without much difficulty) is the proximal tubule.

In the distal tubule, the paracellular paths are tight (due to the presence of tight junctions) and this would prevent water from following Na+ without the help of membrane transporters. It doesn't matter how high the concentration gradient gets if there's no way for the water to follow (an example is the thick ascending LoH that is impermeable to water but actively establishes a concentration gradient by pumping Na+ out). Hope this helps.