- 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
See how ADH acts on blood vessels and the kidney to raise blood pressure. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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- Does the ADH leave the blood system during this process or is it removed elsewhere in the body?(5 votes)
- "Circulating vasopressin has a half-life of 5 to 15 minutes. Endothelial
and circulating endo- and amino-peptidases are responsible for its eventual degradation, and
plasma levels are low under basal conditions. " p.16 - from http://edoc.unibas.ch/609/1/DissB_7925.pdf
This means that all the vasopressin you produce will be reduced to half each 5-15 minutes by the effect of enzymes in the blood and on surface of blood vessels. These are endo- and amino-peptidases mentioned before: they have have this job of non-specific enzymes that break down many small peptides which avoid building up of proteins in the blood.
A similar system to break down proteins is available inside each cell and it is called a proteassome. Actually there are many kinds of proteassomes, but all you need to know about it is that it is kind of like a cell's garbage dispenser or metal shredder.(9 votes)
- Why are blood and urine flowing in different direction?(6 votes)
- this is because of the countercurrent exchange between the peritubular capillaries and the loop of henle/collecting duct to conserve osmolarity gradient(4 votes)
- Ok wait I' m confused now - ADH responds to decreased blood pressure, right, which means that its effect is to raise blood pressure? But I read previously that the effect of ADH was to constrict blood vessels, which I thought would slow down the BP, no? Does constricting blood vessels increase BP? Sorry if it's a stupid question :/(1 vote)
- ADH, antidiuretic hormone is also called vasopressin. It has two main effects, to cause the kidneys to retain water returning it to the systemic circulation and to constrict blood vessels. Both of these actions cause an increase in blood pressure, BP. If the person is dehydrated they have a lower blood volume. By increasing the retention of water, ADH causes an increase in blood volume and that increases blood pressure. Imagine you have a hose and you want to water flowers on the far side of the garden and your hose does not quite reach. If the hose had more water volume, then it would have more water pressure and you can arc the water out further to reach those flowers. Now, imagine you can't turn the up the water volume, what else could you do ? A simple answer is put a nozzle on it and make the nozzle opening small, constrict the vessel. Decreasing the outflow diameter will also increase the pressure and suddenly that water will be a more narrow stream that will reach further so those flowers on the far side of the garden will get watered. ADH does both, increases blood volume and constricts blood vessels to increase blood pressure.. https://en.wikipedia.org/wiki/Vasopressin(11 votes)
- Rishi draws the aquaporins like a ball with the channels attached to it, what happens to the ball?(3 votes)
- The balls are vesicles with the aquaporins embedded on the vesicle membrane. When the vesicles merge with the plasma memebrane of the cell the aquaporins also become a part of the plasma membrane. So the "ball" becomes a part of the membrane.(5 votes)
- When he says the osmo receptors detect salt really they're detecting an increase in osmolarity(osmolality) so it could be from glucose or some other osmotically active solute? Secondly, when he talked about the increase in the salt concentration down the loop how does the salt get there from the blood? What causes the loop to pull the salt out? And, is it always actually salt or can it be some other osmotically active solute? He mentioned the blood flowing in the opposite direction is that because it was venous blood this time? Lastly, what is the driving force to pull the water in to the vessel since the concentration of salt is so high in the collecting duct osmosis would make water want to go in to the collecting duct?(2 votes)
- The osmoreceptors are indeed detecting the Na concentration, they have receptors for Na and if there is more of it running though the tubules, it is more likely to trigger them and have theme release renin.
The salt gets into the renal tubules through filtration in the glomerulus. Most all electrolytes are passively filtered at this stage into the tubules. As the descending loop goes deeper water is actively pulled out and at that point the tubules do not allow the Na to leave. As you reasoned the loop water is passively diffused back into the loop and I. The proximal tubule and distal tubule ADH and aldosterone act to reabsorb some of the water and a lot of the Na creating a dilute urine.
ADH also works on the collecting duct to allow for water reabsorption in the instance that water needs to be conserved.(4 votes)
- ADH is antidiuretic hormone which prevents diuresis but it also causes constriction of blood vessels thus increasing the GFR. Doesn't increase in GFR increase the urine discharge? How can ADH have antagonistic effects?(3 votes)
- What is an aquaporin? It's not a cell, is it? Can a cell be inside another cell?(2 votes)
- how does the water cross the basolateral membrane? do the vesicles with aquaporin also fuse with that membrane?(2 votes)
- The Aquaporins are only on one side, that means the other side is permeable to water.Really simple!(1 vote)
- the collecting duct cell senses the ADH, then the vesicles with the aquaporins fuse with the collecting duct membrane? Are the vesicles always there on the interior? Also, could someone please explain why blood is going the other direction - is it just because its going back to other parts the body and urine will be excreted? thanks!(2 votes)
- can u please explain me simply the relation that when blood pressure increases then what is the effect on ADH and Aldosterone respectively?(2 votes)
We left off the story of antidiuretic hormone when it was just secreted into the blood vessels of the posterior pituitary. So it was just synthesized, just made. It's a little hormone. And ADH was on its way to different parts of the body. So let's just pick up the story right there. And figure out where does it go next. So this little molecule is, we said, a small peptide hormone made up of amino acids. And so I'm just going to draw it here. And this little hormone is going to go off to do a couple of important things. So we know at the end of the day, it really wants to increase blood pressure. So one of the places it visits is all of the vessels of the body, all the arterial vessels of the body. And specifically, it targets smooth muscle. So this hormone is going to go and get this smooth muscle to constrict. And we know that when smooth muscles constrict, the blood vessels are actually going to tighten down, and we call that vasoconstriction. So the blood vessels are going to get tight and small, and that's going to increase resistance. And increased resistance is going to relate to blood pressure. And we'll talk about how we know that. There's that formula. I'm going to write it over here-- delta P equals flow. Q is flow times resistance, is R. And you can actually change that around to say arterial pressure minus venous pressure equals-- and we know the flow is actually stroke volume times heart rate, and it's all multiplied by resistance. So if you look at this, and if we assume for the moment that the venous pressure is going to be basically unchanged, then anything that increases the resistance over here is going to increase our pressure over here. So that's why, in this case, if ADH is able to cause constriction of the blood vessels and increase resistance, our pressure would go up as well. So that's actually one of the things that it does. And the other thing that it does is it's going to act on the kidney. So it's going to have an effect on the kidney. Here's my kidney. And specifically what it's going to do is it's going to cause increased reabsorption of water. So increased reabsorption of water is going to increase our stroke volume. So now you can see the other key effect it's going to have. If it's going to cause your stroke volume to go up, then just as before, now you have an increased stroke volume. So your arterial pressure is going to go up, maybe doubly up. So it's going to cause the blood pressure to go up for a couple different reasons. Now, let's explore this second point in a little bit more detail, the whole idea of how it causes the stroke volume to go up. So for that, what I want to do is I'm actually going to create a little bit of space. And I'm going to draw out, again, as I've done before, the efferent and afferent arteriole. So we know that blood is going to enter the kidneys, and it's going to do this twisting on itself in the glomerulus. And so this is our little glomerulus. And there's the proximal convoluted tubule. And there's the loop of Henley. And this is the distal convoluted tubule, and finally, a collecting duct. So we know that this is basically what the nephron looks like. And I haven't label all the parts, but I'm going to label the important part, which is this part right here. So this area here is the collecting duct. And what I'm circling in blue is what the ADH is actually going to work on. It's going to work on this area, the collecting duct. So it's going to have its effect here specifically. And let me try to draw this a little bit larger so we can see exactly what goes on. So let's imagine that you have, let's say, one cell there. And here's another cell here, something like that. And you have a blood vessel going alongside of it. Now, we haven't actually talked about this before. But down in here-- actually, let me switch colors for a moment. We have urine going this way, and blood going this way. So already, you might be a little surprised. You're thinking, well, why is blood going up and urine going down? That makes no sense. Now, think about this. Before when we were talking about blood and urine flowing in other parts of the nephron, we were kind of separating out the nephron, talking about this top bit. So we were talking about this top bit here. And in here, the concentration is around 300. And actually, the units on that-- I'll just write the units up here-- are milliOsms. So it was around 300, but if you go deeper, it's about 600. And then if you go deeper than that, it's about 900. And if you go down here, it's about 1,200. So what's happening as you go deeper is that it's basically getting more and more salty. So it's getting very salty. I'll actually write that sideways, very salty as you go down. And that saltiness is really, really important, because what it does is it allows us to concentrate our urine. And you'll see why I say that. So keep that saltiness in mind and the fact that there's this big gradient. And I'm going to actually just assume, right now, that we're talking about something, let's say, at the 900 level. So we're at this point right here-- 900 milliOsms. So we've got a pretty salty area out here. Now, as I said, urine is flowing through. And in these collecting duct cells, we have something called an aquaporin that basically sits like this. Let me actually show you what it would look like. So these areas are not going to allow water to go through. That's actually the first point that I want to make. Water cannot go through these areas, except for when there's a little aquaporin channel. And I'm drawing the channels for you. So you can see they're not on the surface, right? So there's no way that water, if water is sitting over here, there's no way that it can actually get through. It would actually just bounce off because it's not able to permeate the cell. It can't actually get in. So water just kind of bounces back and basically goes down into the urine. Now, what ADH does-- and this is the neat thing. So ADH, what it will do, is it will float up. So ADH is actually going to float through the blood, because we said that ADH is going to be all over the body. So this little molecule is going to go through and float by this collecting duct cell. And it's going to have an effect on it. So it's going to have an effect on this collecting duct cell. What it's going to do exactly is it's going to make those little aquaporins. Let me write that out actually. This is an aquaporin. And you can see that's a really easy word to remember because it's literally aqua, meaning water, making a pore for water. So this aquaporin vesicle is actually going to merge with the wall. It's actually going to merge with the wall like that. So let me actually erase a little bit and show you what would happen. So now you have-- instead of this aquaporin sitting out here, you literally have little channels that are now fused in with the wall. So you can see how those little vesicles just bumped right into the wall and fused into it. And now water is going to get a free ride across. It's going to be able to just go right through that channel just like that-- boop-- and into the blood. And it's going to do it again here. And it's going to go here. So all this water is just gushing in to the blood. Look at all this water. And so this blood is going to be loaded with water now, something that it did not have before, because the water couldn't get across before. And so this blood is going to go up, loaded with water, because of the ADH. The ADH basically allowed all that water to finally get across, and the blood is now full of water. +And so now you can see how the volume of blood is going to go up. And if the volume of blood goes up, it's going to create a larger stroke volume for the heart. So that's specifically how the stroke volume goes up.