Health and medicine
- Parts of a nephron
- General overview of the RAAS system: Cells and hormones
- Renin production in the kidneys
- Activating angiotensin 2
- Angiotensin 2 raises blood pressure
- Aldosterone raises blood pressure and lowers potassium
- Aldosterone removes acid from the blood
- ADH secretion
- ADH effects on blood pressure
- Aldosterone and ADH
Learn the key triggers for ADH secretion. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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- What does the optic chiasm do? Is it in any way relevant to ADH production or release?(6 votes)
- Luminoustedium is right. They aren't really related, but they just happen to sit near each other in the brain. The interesting thing is that if you get a pituitary tumor, the enlarged gland can press on the optic nerve and cause partial blindness. The type of blindness is called "bitemporal hemianopsia", which means that you lose sight in the outside portion of your vision in both eyes.(15 votes)
- At4:17there is the whole picture of the Hypothalamus. He said ADH is made there. In class, I learned that ADH made the kidneys stop releasing more water. The hypothalamus made the RH hormone and send it to the Hypofyse. The hypofyse will produce ADH. This is what I learned in class on school. I hope I am clear above but I am confused. I hope someone can explain me where I am wrong.(3 votes)
- ADH is made in hypothalamus and then stored in the posterior pituitary gland. You are correct when you say that ADH acts on the kidneys to decrease water excretion (thereby increasing the amount of water in the blood, which increases stroke volume, which increases total blood pressure), but you are incorrect about the way that ADH gets released: there is no releasing hormone for ADH. Instead, ADH is released in response to one or more of the following:
1) Low blood volume (as in during a traumatic injury with a large amount of blood loss)
2) Low blood pressure (as detected by baroreceptors, aka pressure receptors, in blood vessels)
3) Angiotensin II (as part of the RAAS pathway, used in increasing BP)(12 votes)
- I'm confused about triggers and Na concentrations. Renin is released when the macula densa sense low Na levels but ADH is released when the blood is too salty? Is that because the low levels of salt the macula densa sense means a lot of salt had to be absorbed in the proximal tube and the loop of Henley in order to absorb more water? And this happens because there is a high osmolarity?(5 votes)
- ADH is released when osmolarity is high, too much Na+, because of dehydration. It causes retention of water by the kidneys, and it also causes vasoconstriction in the body to bring up blood pressure.
Aldosterone is released when Na+ is low and K+ is high. It causes the retention of Na+, and water follows the Na+ back into the blood while K+ is put in the filtrate. Both ADH and Aldosterone work on the DCT and collecting duct to retain water. They can work independently of each other.
Renin is released when blood pressure is low (and Na+ is low) in the nephron and it becomes Angiotensin II (2) It causes vasoconstriction and the co-release of both ADH and Aldosterone. All three work to increase blood volume and blood pressure to ensure normal GFR in the kidney. Yes, there is a lot going on. Basically, your body has several ways it responds to low blood pressure, BP, because without oxygen delivery our cells die. If the kidneys are not getting BP they are not getting oxygen AND the blood urea nitrogen, a waste product, is building up in the body.(8 votes)
- At7:42, Rishi says that the body notices that the blood is too dilute. I was wondering how does our body know that our blood is too dilute? Do the Macula Densa cells tell the body?(4 votes)
- One way it could know is the arterial blood pressure, which Rishi describes in the case when ADH needs to be released in response to low blood pressure. When blood pressure is too high ADH is likely inhibited or an antagonistic hormone may be released to bring the body back to equilibrium.(3 votes)
- Whats the difference between ADH and ANH? Just asking cause i am totally new to these terms.(3 votes)
- ADH stands for Anti-Diuretic Hormone, whereas ANH stands for Atrial Natiruetic Hormone. ADH acts to increase water retention and increase blood pressure. ANH acts to decrease blood pressure. ANH, interestingly is a hormone released from the upper chambers (atria) of the heart.(4 votes)
- At the 5 min mark, Dr. Rishi indicated that ADH is carried to the rest of the body via the venus system as opposed to the arterial system? All other nutrients and oxygen are carried via the arterial system.
Is ADH carried to the rest of the body via the venous system?(2 votes)
- It's carried to the rest of the body by the circulatory system, not just the venous portion of the circuit.(3 votes)
- At11:28, Rishi mentions receptors in the large veins. What are the receptors in the large veins called?(2 votes)
- These receptors are still called Baroreceptors and they are mechanoreceptors that react to decreased vessel stretching (or lower volume/pressure). Blood volume, especially on the venous side, helps determine the blood pressure so you can still consider them to be Baroreceptors.(2 votes)
- At3:38, Rishi says that the ADH hormone is 9 amino acids long, but it has the same affect on blood vessels (vaso constriction) as an 8 amino acid-long hormone, angiotensin 2. What is the difference between their effects on a blood vessel? could ADH do angiotensin 2's job if renin cut off 443 amino acids and ACE didn't touch it?(2 votes)
- They probably have different active sites and their "key" nay fit into a different lock which could cause a separate effect. Also, those AA's could be different or in a different order and one change in an AA could create a totally different protein than the previous one(2 votes)
- Do you mean milliosmoles instead of osmoles?(2 votes)
- Hi! Wouldn't salty blood (Increased osmolarity) mean that more water would move into the vessels, therefore increase blood pressure?(1 vote)
- That is correct! Aldosterone does exactly what you described. It increases the Na+ uptake from distal convoluted tubule and during the process, water follows. That means blood has more fluid than previously and will lead to higher blood pressure.(3 votes)
We're going to talk about antidiuretic hormone. And you can see I've already started drawing for this video. And the main reason is because I'm not a great drawer, and I wanted to make sure that everything was pretty clear. And so I drew out on one side the pituitary gland and on the other the brain. And so antidiuretic hormone-- I underlined ADH because that's usually what it's called. People call it ADH. Sometimes people call it vasopressin as well. Actually, vasopressin is good because it's useful. You can see "vaso" kind of refers to blood vessels, and "pressin" kind of squeezing down on blood vessels. It gives you a clue as to what the hormone is doing. So I've drawn for you the hypothalamus here. Also, right below it, this would be kind of the infundibulum, kind of the neck. And at the very bottom, the pituitary. So this is the actual pituitary down here. And there's a front and back to this. And the front, facing forward closer to the eyes, would be the anterior pituitary. So that'd be over here. And back here, this lobe would be the posterior pituitary because it's a little bit further back. And since we're naming stuff, let me just go ahead and round it out. This right here is actually the optic chiasm. It has to do with vision. So I'm just going to write optic chiasm so you know what we're talking about. And the only reason I even bring that up is because just above it-- let's say in this area-- just above it. And if I was to draw it over on my little diagram-- that'd be maybe right there-- is what's called the "supra"-- S-U-P-R-A-- supraoptic nucleus. And nucleus here just refers to a collection of nerve cell bodies, not the nucleus we usually think of-- meaning not the one where it's sitting inside of a cell and kind of directing the flow of traffic in the brains of the cell in a way of saying it. But here the nucleus is actually just a collection of little nerve cell bodies. And I'm actually just going to draw two, but you know there's actually many more there. This is just for diagram purposes. And actually, if I was to draw the rest of this nerve, you would actually go all the way down. And this is actually beginning to share with you some of the cool aspects of this hypothalamus and the posterior pituitary. You can see that, basically, these nerve cells start in one spot, and they go all the way down to the posterior pituitary through that infundibulum. This is how the hypothalamus and posterior pituitary are connected-- through nerves. And these nerves are actually full of the hormone ADH. So we've already talked about the fact that this is related to ADH, but now you can see exactly how. ADH is actually being made in these nerve cells. And it's actually sitting here waiting for the right moment for these nerves to release it. And this ADH is actually a small protein. It's nine amino acids long. So it's actually pretty small. This is ADH. Nine amino acids. So it's pretty teeny, and it's a hormone. And if you know it's an amino acid-based hormone, you can think of it as a peptide or a protein hormone and distinguish it from the steroid hormones. So this is how ADH is made. It's made in these nerve cells. And the next thing to talk about is how it's released. And so if you have, let's say, a little capillary bed in here with little arterials and capillaries coming together into little venules on this side, what happens is that, when there's a trigger-- and actually, maybe I should write that in a very bold color. Let's say red. That's my favorite bold color. When there's a trigger, these nerve cells right here are going to fire off their ADH. They're going to release all that ADH, and it's going to dump right here into this area where all the capillaries are. And of course, the flow of blood is going to carry all that ADH into the little vein-- and let me draw the venule and the vein-- and basically, take it to the rest of the body. So this is how ADH actually gets released out of the nerve cells that live in the supraoptic nucleus and gets out to the body. It basically does it by dumping into that posterior pituitary and getting picked up by all those little capillaries and venules. So I guess the next issue is to figure out what is the trigger? So what is the trigger for this little supraoptic nucleus that I've drawn here? So let's talk about that. Let me make some space. There. Now, we've got a clean bit of canvas. So let's talk about the triggers that our body uses to know when to fire off that ADH to get it released. The main trigger-- and this is probably the one trigger that you want to take away. If you're going to forget everything else, try to remember this one. The main trigger is going to be high blood concentration. And the way we think about blood concentration is in osmolarity. Let me write that down. What osmolarity refers to is, if you took all the solutes that are floating around in the blood-- so that includes everything from protein to sodium to potassium, everything that is going to drag water into the blood vessels-- if you combine all that, then what is your total blood concentration going to be? And you can almost think of it as a meter. So let me draw it for you. Like a little meter here. On one side, you've got-- let's say something like that. And on one side, let's say you've got 260, and on the other side 320. And this is just concentrations. So 280 and 300. And this is osms per liter. And actually, these are the units here. So osmolarity as measured in osms per liter. So this is the concentration. And what you want to do is you want to really stay in this area right here. This is kind of your green zone. This is where the body likes to be, generally speaking. And if it's here, if it's in this area, or if it's in this area, then that's where the body is not too happy. And so for example, let's say you're in this first zone. This would mean that your body is noticing that the blood is too dilute. And if it's on this side, your body's noticing that it's too salty. The body is saying that the blood is too salty. And so in this case, if you have, let's say-- like I said-- a meter down here, if the needle is falling in this area, then that's going to be a trigger for ADH release. So that's the first trigger that we can talk about. In fact, why don't I even go back up and add that to our diagram? So I'm going to put that into our diagram so that we can see it very clearly as being one of the triggers. So let's imagine you have right here a little nerve cell. And I'm going to draw it this way purposefully because we actually don't know where these little osmoreceptors are. All we know is that they do a fantastic job, but we don't know exactly where these osmoreceptors are. And this is my little diagram that I drew before. And you can now think, if the osmoreceptor is telling you that it's over there, then that's a problem. And in fact, why I don't I even go one step further and label this as my osmoreceptor? So if my osmoreceptor is set to tell me that it's too salty, that is one of the signals that's going to trigger ADH release. OK. So now, what's the second trigger? What's another reason why we might release ADH? Low blood volume. Think about that for a second. How in the world would your body even know that the blood volume is too low? Well, let's go back to basics. Let's go back to the heart. That's where I like to begin because that's how I always think about it. Just very simply, what is going into the heart, and what's coming out? Well, we know we have blood vessels-- large ones, in fact, large veins-- dumping into the heart. So we have the superior and inferior vena cava. This is the superior vena cava-- this is a large vein-- and this is the inferior vena cava. These aren't the only large veins, but these are two examples of large veins. And we also have the right atrium. So we have a couple of spots here that are in the blood vessels where we might have little nerve endings. So nerve endings in these areas are going to start recognizing when the blood volume is low. Because, remember, the venous system-- this is kind of a stretch-- the venous stretch from something we talked about a long time ago. The venous system is actually going to be a large volume system. So if there's ever a decrease in the volume, that would be one of the best places to figure it out. So information in the walls-- so basically, these nerve fibers, rather, in the walls of the vessels are going to be less stretched. And they're going to say, well, why are we less stretched? And the answer is that there's actually less blood volume. So when they're less stretched, they're going to send a signal and say, hey, something's up. We have less blood volume, and I think the brain needs to know about that. So that's how a signal gets sent all the way up to the brain. And actually, I can draw that in as well. So let's put in a little receptor here. And now, these are going to go down and sense low volume from those receptors in the large veins and the right atrium. OK. Now, what's another trigger? You can see there are a lot of different triggers. I'm putting up one after another. Let's put another trigger up there. What's another reason why ADH would be secreted? Well, maybe a decrease in blood pressure. Now, we know that the veins tell us a lot of information about volume. So it might extend that the arteries can tell us about pressure. And you might recall from another video where we talked about baroreceptors that this is a fantastic way to get information about pressure. So let me draw some of those baroreceptors. And baroreceptor just refers to pressure receptor. We have baroreceptors that are in the aortic arch right there. And we also have baroreceptors that are in the carotid sinuses on both sides. So these baroreceptors are going to recognize when the blood pressure is starting to go low. And they're going to send a signal up to the brain to say, hey, again, we need to do something about this. Our pressure is low. So that's another signal up to the brain. And that we can draw it right here. We could say, OK. Maybe something like this. And that would be a signal about low-- let's write that here-- low pressure. So now we've got signals about high osmolarity, low volume, low pressure. Are there any other signals that we can think of? One more jumps to my mind-- angiotensin 2. Remember, angiotensin 2 is actually part of the whole RAS system-- the renin-angiotensin-- or I'll just write AT-- aldosterone system. And so angiotensin 2 is actually going to be another trigger. So you can actually imagine through a blood vessel, and you might have a nerve nearby. And this is going to trigger right here this molecule of angiotensin, which has eight little amino acids. It's going to be a signal to that nerve that it needs to let the body know-- or the brain know, rather, that pressures are low. This is another signal. And let me just write that up here in our picture. Another signal could be something like this. Maybe right here. And the exact location that I'm drawing is actually just kind of arbitrary, but the idea is that you have angiotensin 2 having effects on the brain as well. So this little molecule is going to come and let the brain know that, hey, even the kidneys are trying to do something about the blood pressure. And it would be great if the brain got involved in releasing some ADH, if needed. So these are the different triggers. And like I said in the beginning, probably the main one you want to think about-- as far as ADH is concerned-- is this osmoreceptor. This is really the most important one because everything else is secondary to that. That is definitely the major function of ADH.