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Aldosterone and ADH

Find out how Aldosterone and ADH cause changes in volume and osmolarity. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.

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  • leafers seedling style avatar for user Jessica
    At around , maintaining volume while decreasing osmolarity is needed and you said aldoesterone should be slightly decreased while ADH is increased. However, ADH release is stimulated by angiotensin 2 and doesn't that also stimulate aldosterone release? Just slightly confused. Thanks
    (18 votes)
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    • leafers ultimate style avatar for user Sleuth
      That can be done with competitive antagonists like spironolactone.
      Aldosterone has to activate a receptor by binding to it. It only activates the aldosterone-receptors because it fits in there perfectly like a key in a lock. Spironolactone has a very similar structure to aldosterone so it will fit in the same receptor but it is slightly different so it won't activate the receptor.
      But since it fits in the receptor it now blocks aldosterone from getting to the receptor to activate it.
      Like a wrong key jammed into the keyhole.
      If a lot of receptors are now blocked it means less aldosterone can activate them which is the same effect as having less aldosterone in the blood because that would also leave less receptors activated.
      And that way you don't have to care about angiotensin 2.

      Spironolactone is a synthetic drug used to lower blood pressure.
      I hope you now see why.
      By the way; good way of connective thinking!
      (25 votes)
  • blobby green style avatar for user virtuosointhemaking
    A few questions-
    1) I noticed in the past several videos it's been mentioned that ADH acts in areas of the nephron that aren't permeable to water (by docking aquaporins on the apical membranes to subsequently render them permeable to water) and aldosterone acts in areas that aren't permeable to water....BUT it was also stated that they both act on the collecting duct...so, what gives?

    2) The action of aldosterone on both principal cells (moving of Na+ into bloodstream and K+ into urine) was mentioned but the action of ADH was depicted as the docking of an aquaporin onto the apical surface of a generic collecting duct cell (thereby allowing for osmosis of water across the cell and into the hypertonic blood)...it's my understanding that collecting duct cells are either principal cells or intercalated cells (alpha or beta)- which type of cell(s) does ADH act on?
    (20 votes)
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    • duskpin ultimate style avatar for user wezh24
      From what I've read in texts, it is actually accurate that both ADH and ALDO act on the collecting duct, but they act on different parts of it. If you might recall from the “ADH effects on blood pressure video”, it is mentioned that ADH acts on parts of the collecting duct that are submerged in the renal medulla where the osmolarity is very high, making aquaporin insertion effectively able to pull water out from the urine / filtrate. In contrast, ALDO acts on the late distal tubule and early section of the collecting duct which runs through the renal cortex rather than the medulla.

      As a slight disclaimer, I've also read some information stating that ADH acts in the distal tubule and early collecting duct. But it still makes sense that the primary region of ADH activity is in the medullary collecting duct, since the other regions don't have the required osmolarity to allow for comparatively effective water reabsorption.

      Unfortunately, I wasn't able to find out what types of cells ADH acts on.
      (10 votes)
  • male robot hal style avatar for user Yuri Sakhno
    At , cannot water go backwards through the same channel? These channels aren't one-way only, are they?
    (6 votes)
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    • leaf green style avatar for user Ege Ülgen
      No they are not. The pores only allow water to diffuse from the hypotonic filtrate into the hypertonic blood in the ascending vasa recta through the normally non-water-permeable tubule walls. ( i.e. ADH just induces the insertion of the pores (aquaporin 2) and the rest of the process is merely driven by the osmotic difference)
      (13 votes)
  • blobby green style avatar for user felahi3
    Because caffeine and alcohol cause dilute urine by inhibiting ADH, does that mean those two substances cause a decrease in blood pressure?
    (5 votes)
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    • orange juice squid orange style avatar for user Alex
      Taken alone that would seem to be the effect, but both alcohol and caffeine have pretty complicated mechanisms of action on the body. In normal or moderate doses, caffeine consumption actually leads to a temporary increase in blood pressure and alcohol consumption has no effect on blood pressure.
      (4 votes)
  • winston default style avatar for user David
    In the last scenario, decrease osmolarity but maintain volume, Rishi says that we should decrease aldosterone, but how does our body decrease the levels of aldosterone if there is no aldosterone at all?
    (5 votes)
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  • blobby green style avatar for user Rodriguez Karen
    I have Addison's disease, I have zero ACTH. At the moment the ER is telling me my potassium is low and my blood pressure has been Dangerously high like, 200/120.
    Why and what can I do to bring my BP down to normal while at the same time bring my potassium up to normal as well?
    (3 votes)
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    • hopper cool style avatar for user Madeliv
      I'm sorry to hear that you are ill. It is however, not recommended to ask medical advice here, and it would be safest to ask these questions to your doctor. You have no way of verifying what somebody posts here. I wish you the best of luck and hope you will feel better in the future.
      (6 votes)
  • blobby green style avatar for user eliz
    If someone has arteriosclerosis, why would they have elevated levels of aldosterone and decreased levels of ADH?
    (2 votes)
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    • blobby green style avatar for user mkjaraki93
      This is my take on the question and I hope it presents some clarity:

      Arteriosclerosis may, especially if focused within the renal artery, reduce blood flow to the Juxtaglomerular cells of the kidney which then perceive a scenario of reduced blood pressure. The kidney JG cells will thus respond to this and release Renin, triggering Angiotensin I formation from Angiotensinogen. Angiotensin I will be convertd by ACE (Angiotensin-Converting Enzyme) to Angiotensin II which induces vasoconstriction and raises blood pressure (via direct action on vascular smooth muscle). It also, more importantly induces the Zona Glomerulosa cells of the Adrenal Cortex to produce Aldosterone.

      The Aldosterone will trigger hyperbolized (increased) sodium resorption from the distal kidney tubules in exchange for potassium and protons (H+) followed by the passive resorption of water as well. Hence, blood osmolarity remains UNCHANGED (recall that hypernatremia or high sodium content or high osmolarity in the blood will trigger ADH release) but the blood volume is effectively INCREASED. For ADH to be relased from the posterior pituitary, either LOW blood volume (hypovolemia) or HIGH sodium concentration must be present. In this case, we have almost the opposite: HIGH blood volume and fairly UNALTERED Na+ concentration. Hence ADH is DECREASED because of the effects on Aldosterone.

      Now, some may ask why the Angiotensin II that triggered aldosterone release didn't cause a visible increase in ADH as well (Angiotensin II can increase ADH as some other comments had noted).
      My guess is that its primary effect is on Aldosterone and that it's effect on ADH is comparatively less. Also the increased volume (even by what little ADH is produced to allow further water resorption from the collecting duct) will serve to suppress it further (part of a negative feedback).
      (6 votes)
  • blobby green style avatar for user rohitrocks1729
    Do Sodium-Potassium pumps in the principal cells use ATP? If so, is it similar to active transport?
    (3 votes)
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  • aqualine ultimate style avatar for user SULAGNA NANDI

    For scenario 4, can someone let me know if I understood properly:

    1. decrease in aldosterone --> Na+ goes from blood to principal cells to filtrate --> H2O goes from blood to principal cells to filtrate through osmosis --> decreased blood volume

    2. increase in ADH --> more aquaporins on apical membrane created --> H2O goes from filtrate to principal cells to blood --> blood volume increases --> blood concentration/osmolarity decreases

    net change in blood volume = (decrease to due aldosterone)+(increase to due ADH) = 0

    net change in blood osmolarity = (no change due to aldosterone)+(decrease due to ADH) = overall decrease
    (3 votes)
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  • aqualine ultimate style avatar for user Mack
    Do both ADH and Aldosterone increase blood pressure?
    (3 votes)
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Video transcript

We're going to compare Aldosterone and ADH or Antidiuretic Hormone side by side. To do this I think it would be helpful if we just do a little recap on how these two work because it's going to help inform exactly what they do. So if we have a little nephron here, a little tubule, and these are the cells lining the tubule and it's going to eventually send the urine on its way out. Next to it I have a little blood vessel, and just to save myself from drawing it twice I'm going to cut and paste this over to this side right here. In this tubule we know that on one side, on the aldosterone side, we have water permeability. This membrane that seperates these two, these layer of cells are water permeable. Over here on the ADH side, we know that they are NOT water permeable. The reason I'm saying it's different is because we know that, although they look the same these are different parts of the nephron. The way that aldosterone works, the main thing it does, it's going to pull in sodium and spit out into the urine potassium. That's the main activity of aldosterone in terms of capturing sodium and what happens is that sodium, we know, is not permeable to membranes. Not able to cross membranes very easily. That's actually really important because if it can't cross membranes, then that means that it's going to contribute to tonicity because we know that the ions that cannot cross membranes are the ones that are the biggest contributors to tonicity. In fact, this is actually very important because potassium by comparison can "slightly" cross membranes. So if you have one ion that cannot cross membranes at all and you give away the ion that can slightly cross membranes, then your tonicity goes up because overall you're getting more ions that can stay in the blood vessel and because they can stay in the blood vessel, it can contribute to tonicity. Water is going to be driven into the blood vessels. So that's really how aldosterone is dragging water into the blood vessel through increased tonicity. By comparison, the ADH is just using water channels if water is unable to get across otherwise, if you through in some water channels then you have no problem gathering water. So these are the key differences: one of them uses an osmole to drag water across and that's why we always say "Water follows sodium." and the other is just using channels. Let me make a little bit of space here. . . let's see if we can create some space down here I'm going to create two categories: one category is Volume and the other is Osmolarity. We know osmolarity actually is simply a fraction. It's just osmoles divided by volume. We have the same thing in the other column and I'm going to do that for this side as well: osmolarity is osmoles divided by volume. We're going to see how these two work and whether one or both will be effected by the hormones. We know that the way that aldosterone works is by raising the osmoles. It's going to change this, going to increase the osmoles and as a result it will increase the volume. So actually, both osmoles and volume are effected. Let me start out by just circling this box because we know that the volume is effected. because osmoles and volume are both affected and that they're proportional to one another we usually don't think of osmolarity being effected by aldosterone because both the numerator and denominator are going to go up if there's a lot of aldosterone or down if there's not any aldosterone around. So osmolarity doesn't really get effected by aldosterone. Now, ADH is a little different. In ADH we have volume going up, that's really the primary thing that's happening So we'd say we have a volume change here but in terms of osmoles, you haven't really changed the osmoles with ADH, not directly. If you haven't changed the osmoles and you have changed the volume then osmolarity is changed. If you just change the denominator, but not the numerator then the number will change. So that's why ADH effects osmolarity although it doesn't effect osmoles. Kind of a tricky thing, but I think you can see it now that the numerator doesn't change, but the overall fraction does. So you have on this side increased volume and you have increased volume on this side and you have decreased osmolarity. So these are the major changes from these hormones. Let me make a little bit more space and we'll continue this line of reasoning. So if these are the changes, now imagine the scenario where you want to increase volume, but maintain the osmolarity. So if you want to increase volume, but maintain osmolarity which hormone would you use? because we can't see the hormone [drawings above], let's just use aldosterone and ADH and I'll just put "up" arrows and "down" arrows These are the two hormones, I want to increase volume, I would definitely use aldosterone because it doesn't effect osmolartiy, but I would NOT use ADH I'll put a little circle with a line through it. I would NOT use ADH because again, I want to maintain osmolarity I would not want to use ADH in that scenario. Now let's say you wanted to increase volume, REGARDLESS of osmolarity meaning you don't really care if osmolarity changes and this could be, let's say you have a big car accident and you're bleeding out and the only thing you really care about right away is increasing your blood volume, that's the only thing that matters, so you really want to increase volume and you want to do it fast. Well, in this scenario, you definitely want to use everything that's available to you, aldosterone and ADH. The fact the osmolarity will go down with ADH really doesn't matter because we said regardless in this scenario so because of that, I'm going to imploy ADH this time. You can kind of get a sense for how this is going to work, right? Now let's say you wanted to decrease osmlarity regardless of volume, so I don't really care if the volume changes a little bit here or there, so in this case, regardless of volume, what would I do? Well, if I didn't really care about the volume and I just wanted to decrease osmolarity that seems like a no brainer, right? That's exactly what ADH will do, it will decrease osmolarity and really in this case, I don't need aldosterone. I said in my phrase here that I don't care about volume changed so, that's fine I'll just use ADH and I'll tolerate the increase in volume. In the fourth scenario, let's say you want to decrease osmolarity and maintain volume, you don't want it to go up or down. This is kind of a tricky one right? because to decrease osmolarity, only one hormone will do that so you've got to start with some ADH, but if you want to maintain volume you know that ADH will cause your volume to go up a little bit and if you don't want it go up, you wanted to maintain volume, you may actually have to decrease aldosterone just a little smidge so that would maintain your volume. Now you can see how the two hormones basically have to work together to get the different outcomes. Depending on what your volume status is and what your osmolarity status is. I can flip around all the arrows or I could say well what about decreased volume and maintained osmolarity or decreased volume regardless of osmolarity? and you would basically just do the opposite of all these things. Any tweak in volume and osmolarity can help you predict what the aldosterone and ADH will be doing.