Aldosterone, just to clarify its effect.

[hellocubed]

So from reading EK it seems that Aldosterone only raises Na* reabsorption in the ascending look and the distal tubule.

I was wondering where wter returns from cause both these tubes are impermeable to water.
The collecting duct? Collecting tubule?? Just as a system in general??

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[MedPR]

So from reading EK it seems that Aldosterone only raises Na* reabsorption in the ascending look and the distal tubule.

I was wondering where wter returns from cause both these tubes are impermeable to water.
The collecting duct? Collecting tubule?? Just as a system in general??

I don't know about the ascending loop, but aldosterone does act in the DCT to increase Na+ reabsorption and K+ secretion. DCT and the collecting duct are both permeable to water because of ADH; I don't know who told you that they aren't.

Also, the effect of aldosterone is to regulate blood volume, while ADH functions to regulate osmolality.

 

[underscore]

The descending limb of the loop of Henle is permeable to water; everything else is impermeable.

Vasopressin/ADH acts in the collecting ducts to insert aquaporin 2 - water channels - into the nephron and allow the reabsorption of water.

 

[underscore]

I don't know about the ascending loop, but aldosterone does act in the DCT to increase Na+ reabsorption and K+ secretion. DCT and the collecting duct are both permeable to water because of ADH; I don't know who told you that they aren't.

Also, the effect of aldosterone is to regulate blood volume, while ADH functions to regulate osmolality.

No, ADH responds to low plasma volume, increased plasma osmotic pressure, and a hormone of the GI tract.

 

[MedPR]

No, ADH responds to low plasma volume, increased plasma osmotic pressure, and a hormone of the GI tract.

No, ADH responds to changes in osmolality, and aldosterone responds to changes in blood volume.

High blood osmolality = stimulate ADH secretion.
Low blood osmolality = inhibit ADH secretion.

Low blood volume = low blood pressure = secrete renin = angiotensinogen -> angiotensin 1 -> angiotensin 2 = secrete aldosterone = increase blood volume = increase blood pressure without changing osmolality of blood or filtrate. ADH too, but who cares

 

[MedPR]

The descending limb of the loop of Henle is permeable to water; everything else is impermeable.

Vasopressin/ADH acts in the collecting ducts to insert aquaporin 2 - water channels - into the nephron and allow the reabsorption of water.

The DCT and the collecting duct are both permeable to water, ADH just increases the permeability. Aquaporin-3 and aquaporin-4 are in the basolateral membrane, while ADH acts on the DCT and collecting duct to promote the insertion of aquaporin-2 on the apical membrane.

 

[loveoforganic]

In normal physiological situations, aldosterone is the primary response for regulating fluid volume, and ADH is the primary response for regulating fluid osmolarity. Significant fluid loss is a very potent stimulus for ADH release, however. And they're both stimulated by angiotensin II

Edit: I was under the impression the collecting duct was essentially impermeable to water sans ADH. The AQP3/4 transporters have no water to transport unless it has a non AQP2 route across the apical membrane

 

[chaser0]

And they're both stimulated by angiotensin II

Whoa angiotensin II stimulates aldosterone AND ADH?
Both the Kaplan MCAT Biology book and the Exam Krackers Biology book. only note Aldosterone.

 

[loveoforganic]

Yes, but less important response than aldosterone, which makes sense based on the mechanism for JG renin release (decreased concentration of NaCl through DCT passing the macula densa - wouldn't be intuitive for ADH due to low osmolarity representing high fluid status)

 

[Charles_Carmichael]

No, ADH responds to changes in osmolality, and aldosterone responds to changes in blood volume.

High blood osmolality = stimulate ADH secretion.
Low blood osmolality = inhibit ADH secretion.

Low blood volume = low blood pressure = secrete renin = angiotensinogen -> angiotensin 1 -> angiotensin 2 = secrete aldosterone = increase blood volume = increase blood pressure without changing osmolality of blood or filtrate. ADH too, but who cares

Hypovolemia (loss of blood volume) is actually a strong stimulus for ADH release. In fact, when there's hypovolemia, ADH release is even more sensitive to changes in plasma osmolality. Think about it intuitively: another name for ADH is vasopressin -- the name tells you that it can act on blood vessels to affect blood pressure. And blood volume is directly tied to blood pressure.

The general idea though is that the RAAS is predominantly involved in blood volume regulation while the ADH mechanism is predominantly involved in regulation of plasma osmolality. The key word there is 'predominantly', not 'only'. My point is just that don't be so absolutely set on wherever you're reading some of these things and passing them off as facts, especially if your source is an MCAT review book. They tend to cover only the bare basics. Not a knock on you; I just wanted to point out that everything's more complicated than "X does only this, while Y does only that." Once you get to med school, you'll see.

The DCT and the collecting duct are both permeable to water, ADH just increases the permeability. Aquaporin-3 and aquaporin-4 are in the basolateral membrane, while ADH acts on the DCT and collecting duct to promote the insertion of aquaporin-2 on the apical membrane.

In normal physiological situations, aldosterone is the primary response for regulating fluid volume, and ADH is the primary response for regulating fluid osmolarity. Significant fluid loss is a very potent stimulus for ADH release, however. And they're both stimulated by angiotensin II

Edit: I was under the impression the collecting duct was essentially impermeable to water sans ADH. The AQP3/4 transporters have no water to transport unless it has a non AQP2 route across the apical membrane

+1

Also, you're right that the collecting duct is essentially impermeable to water in the absence of ADH-stimulated AQP insertion. As far as I'm aware, without ADH, there's pretty much no reabsorption of water in the collecting duct/late DCT. That's why in diabetes insipidus (lack of ADH release or function), there's massive loss of water.

 

[MedPR]

Hypovolemia (loss of blood volume) is actually a strong stimulus for ADH release. In fact, when there's hypovolemia, ADH release is even more sensitive to changes in plasma osmolality. Think about it intuitively: another name for ADH is vasopressin -- the name tells you that it can act on blood vessels to affect blood pressure. And blood volume is directly tied to blood pressure.

The general idea though is that the RAAS is predominantly involved in blood volume regulation while the ADH mechanism is predominantly involved in regulation of plasma osmolality. The key word there is 'predominantly', not 'only'. My point is just that don't be so absolutely set on wherever you're reading some of these things and passing them off as facts, especially if your source is an MCAT review book. They tend to cover only the bare basics. Not a knock on you; I just wanted to point out that everything's more complicated than "X does only this, while Y does only that." Once you get to med school, you'll see.


+1

Also, you're right that the collecting duct is essentially impermeable to water in the absence of ADH-stimulated AQP insertion. As far as I'm aware, without ADH, there's pretty much no reabsorption of water in the collecting duct/late DCT. That's why in diabetes insipidus (lack of ADH release or function), there's massive loss of water.

Yes, ADH does respond to low blood volume, but its primary purpose (for the MCAT) is osmolality regulation, while Aldosterone is blood volume. I'm well aware that there is much more to it than discussed in my previous posts, but this is the MCAT forum, not the USMLE forum.

 

[underscore]

Yes, ADH does respond to low blood volume, but its primary purpose (for the MCAT) is osmolality regulation, while Aldosterone is blood volume. I'm well aware that there is much more to it than discussed in my previous posts, but this is the MCAT forum, not the USMLE forum.

I may be naive, but I'd really hate it if the MCAT were explicitly wrong/misleading.

 

[MedPR]

I may be naive, but I'd really hate it if the MCAT were explicitly wrong/misleading.

It's not misleading, it is just that the MCAT requires only superficial knowledge. An overly simple example is your legs. The primary purpose of your legs is to allow you to stand upright and to be able to walk. Obviously, however, you can kick someone and use your leg(s) as a weapon in specific situations. Analogously, ADH primarily acts to regulate osmolality, but when necessary will respond to changes in blood volume as well.