- Renal regulation of blood pressure questions
- Mini MCAT passage: Denervation of the renal artery
- Mini MCAT passage: Syndrome of inappropriate antidiuretic hormone
- 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 Aldosterone effects the principal cells of the kidney to raise BP and lower potassium. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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- At12:40, Dr. Desai states that increased water leads to increased stroke volume which leads to increased blood pressure. I don't understand this. If increased water means increased systemic volume then I could see increased filling of the RV from the RA either through initial passive filling or RA contraction. This increased filling of the RV would then possibly lead to higher pulmonary pressure and return to the LA which would lead to increased filling of the LV and then greater stroke volume. But if that is the case then it is the increase in water initially that is what is increasing the blood pressure which then increases stroke volume, no?
so instead of H2O ---> SV ---> BP
isn't it really H2O ---> BP ---> SV?(10 votes)
- The pressure in this case is referring to the sum total of the pressure in all the vessels in the body, and not just specifically where the water is being resorbed. This is how it breaks down in more detail:
Increase H2O reabsorption --> Increase blood plasma volume --> Increase blood volume --> Increase venous return to heart --> Increase end diastolic volume (EDV) --> Increase stroke volume (SV) --> Increase cardiac output (Q) --> Increase mean arterial pressure (P)
P = Q x R
Q = HR x SV
Hope that helps!(36 votes)
- Please excuse my ignorance. This series of videos keeps highlighting the body's methods of INCREASING blood pressure, but I'm left to ponder the idea of why? I've always assumed high blood pressure was a physiological catastrophe, so why would the body want to put our "system" under so much undue/undesired stress? Thx in advance!(6 votes)
- Because low pressure is very bad. You need to maintain a stable blood pressure in order to keep your organs supplied with oxygen. If your blood pressure drops too low you will be weak and dizzy, you may lose consciousness and will eventually go into shock and die if it is not corrected.
Being able to increase your blood pressure is a very important survival mechanism.(11 votes)
- Why is it that water follows Na+ ions but does not follow K+ ions?(10 votes)
- Water follows both ions, but it'll follow the ion that there is more of in the blood stream (Na+). High concentrations of K+ in the blood stream is toxic, so the kidneys need to get rid of it or store it inside cell cytoplasm.(6 votes)
- At7:52, Rishi says that sodium is the main solute in the blood but aren't red blood cells the main solute in blood?(5 votes)
- Cells can't be a solute. When we talk about solutes in blood we usually refer to the plasma, which is the portion of the blood excluding cells. Also, cells don't exactly dissolve in water because they're too big.(11 votes)
- So aldosterone increases the concentration of Na+ ions in the blood, which in turn causes water to "get pulled into the blood?" At4:45, Rishi says that aldosterone works in the late distal convoluted tubule, which, I thought is impermeable to water. Does this mean that aldosterone (or maybe ADH?) creates water channels in the principal cells to allow the passage of water? Or is this part of the nephron actually permeable to water? Thanks!(4 votes)
- Yes, you are right. Both ADH from the posterior pituitary and Aldosterone from the adrenal cortex are released if blood pressure is too low. Both cause 'aquaporins' or water pores to be inserted into the distal convoluted tubule and the collecting duct of nephrons. Aldosterone is also released if plasma sodium is too low since it also causes the reabsorption of sodium ions. Increasing blood volume improves blood pressure and feeds back on their respective glands to reduce the hormones release. Hormones act on cells and change their activity or characteristics. Without these hormones in particular, our urine would be dilute and high volume and we would be drinking water like crazy. PU/PD, Polyuria/polydypsia would be on the chart! You get it!(4 votes)
- This is minor, but in another video, they highlighted that blood and urine flow in opposite directions.
At6:50, he drew the blood flow and urine flow in the same direction. Like I said, it's a minor detail but throws off a lot in the function of the kidney re-absorption.(5 votes)
- How does the level of potassium ions increase in the blood?(3 votes)
- Sometimes there is a high intake of potassium in the diet. Other times, the kidney fails to remove potassium from the blood, due to renal failure or certain medications which block the proteins that help us excrete potassium, e.g. Spironolactone(3 votes)
- Aldosterone works on the distal convoluted tubules and collecting ducts causing sodium to rush in to the cell and water follows, isn't it impermeable to water or does aldosterone make aquaporins?(4 votes)
- My teacher has written on her powerpoint that when you have respiratory acidosis H+ leaves the cell in exchange for K+. Can someone explain why? She has written that it's a dilution. I don't know if it's a accurate translation but in swedish (the language i study medicine in) she has written "spädning": dilution. Thanks for the help!(3 votes)
- Basically, this is part of the cell's attempt at buffering the acidosis. Remember that there are two main acid/base buffer systems in the body: respiratory and metabolic. In the case of respiratory acidosis (when you're retaining too much CO2 leading to decreased levels of bicarbonate in the blood which decreases pH), one major way that the body responds is to attempt to dilute the amount of free H+ by exchanging intracellular K+ for the extracellular H+. This becomes clinically relevant because of the effect on perceived K+ levels both during and following pH normalization.(3 votes)
All right, we've talked about renin, we've talked about angiotensin. Let's talk about aldosterone now. Aldosterone is the final hormone that gets your blood pressure to go up. And so where does it come from? Aldosterone comes from a gland. I'm going to draw it here. And the gland is actually called the adrenal gland. And this gland literally sits right on top of the kidney. And so let me draw the kidney here for you so you can kind of orient yourself to where this gland would be sitting. And, of course, you have two kidneys. And you have two adrenal glands. You have the left and the right. And if you were to look inside of the adrenal gland, you'd notice that, actually, in the middle of the adrenal gland is an area that looks different than the outside. And we call that the medulla. The inside is the medulla. And the outer bit is the cortex. And they make different hormones. And this cortex is actually the part of the adrenal gland that makes the aldosterone. So let me draw some cortex cells here for you. And in the middle is a blood vessel kind of running through. I'll draw that in just a moment. So these cortex cells are basically like any other cells. They need food, they need nutrients, they need oxygen. And so these capillaries that are running through are going to provide all of that to these cortex cells. And if you were to take a microscope and, let's say, look deep within these cells. Maybe not even with a microscope, but let's say you were able to look deep within these cells, you'd notice that there is cholesterol in these cells. So there's cholesterol sitting inside of the cells. Actually, not visible, but it is there. And the cholesterol, I've always wondered, what is the point of cholesterol? It always seems like it's a bad thing. This cholesterol is actually really useful to these cells because it helps them make the hormone aldosterone. Actually, aldosterone comes from cholesterol. And if you put the molecules next to each other, you'll see how similar they are. They actually look really, really similar. So these cells are the ones making aldosterone. But, of course, you can't just make aldosterone willy-nilly, you have to wait for the right moment, right? So when does that cell know to make aldosterone? What are the triggers? Well, there are a couple triggers. One would be if you see, or if those cells encounter angiotensin II. So if angiotensin II comes around, that would be one of the triggers to let the cholesterol turn into aldosterone. Angiotensin II, you remember is floating through the body. It's actually quite a journey of its own, making its way from the liver initially and all the way into meeting renin and then meeting angiotensin converting enzyme. So this angiotensin II has been around a long time and it finally makes its way to the cortex of the adrenal gland. And it is one of two stimulus for making aldosterone. And the other stimulus is actually not a hormone, but it's actually the ion potassium. So you know blood has a lot of sodium in it, but it also has a little bit of potassium in it. And if those potassium levels start creeping up, if you have a little bit too much potassium, then that is a stimulus for getting some aldosterone out there in the blood. So these are the two triggers for getting cholesterol into aldosterone. So just keep that in mind. And let's actually now make a little space on our canvas and see exactly where the aldosterone works and how it works. So let me scroll down. And let's go back. Let's think back to our blood vessel that enters the kidney. And we know that we call that the afferent arteriole and it goes into the glomerulus, which is that little clump of blood vessels I just drew there. And the afferent arteriole and efferent arteriole, this is all review now, right, are in the kidney. These are the blood vessels that have entered, and the efferent arteriole is exiting the glomerulus of the kidney. And remember, this is our little kidney nephron. The Bowman's capsule, and the proximal convoluted tubule, and we have that Loop of Henle. And we have that distal convoluted tubule that goes like that. And then it all kind of comes together in the collecting duct. So this is the nephron, right? This is our image of the nephron. And now to answer the question of where does aldosterone work, I needed to draw this because I wanted to show you that it actually works in this area that I'm circling in blue. So this is kind of the area that the aldosterone is working on. And right here, this part right here, is the late part of the distal-- so I'll call it the late distal convoluted tubule. And the other part that it works on right here, is the collecting duct. So these are the two areas that the aldosterone is actually going to have an effect on. So it's going to affect the kidneys. And it's actually going to also effect the gut, but I'm not going to get into that too much detail because the main effect of aldosterone is on the kidney. And so let's try to blow up some of these areas so you can see exactly what I mean. Let me draw a cell here. Here's one cell. And just imagine that you've got another cell there and another cell there. And you've got, let's say, a few cells there. And they're lining the nephron, right? They're lining the, let's say, the distal convoluted tubular, or the collecting duct. And these are called principal cells. And it's actually spelled the way that a principal at a school would be called or spelled. So this is a principal cell. And on the other side of it, over here, you've got blood flowing. And you remember we talked about the peritubular capillaries? Well, this is where it comes into play. Peritubular capillary is actually sitting next to the principal cell, and blood is flowing through here. And, of course, this is filtrate. Or what will soon be urine, is flowing through here. So we've got blood and urine flowing through. And we've got a couple of surfaces here, right? So we've got one surface here. And this is called the basolateral surface. And this becomes really important because the surfaces are where ions are going to be dancing back and forth. And this is the other surface, this is the apical surface. So this is the surface between the principal cell and the filtrate, or the urine. OK, so we've got a couple surfaces, we've got a cell, and we've got some blood and urine. And now you remember that most of the inside of the cells is going to be loaded with potassium, right? So there's a lot of potassium in here. And if this is another principal cell, there's more potassium in here. And the blood is going to have a lot of sodium. So let me draw sodium over here. So a lot of sodium in the blood. That's the main solute. And a lot of potassium in the cells. And now these aren't the only ions in the blood or in the cells. These are the main ion in the blood and cells. So just keep that in mind. They're not the only ones, but they are the dominant ones. And so what happens is that the cells want to maintain this gradient, right? This is always the case. They always try to maintain this gradient. And they have this wonderful sodium potassium pump to do it, right? They have this pump that basically gets two potassiums over here, and it squeezes three sodiums out over here. Right? So we have this sodium potassium pump. Three sodiums. And this pump does not come for free, right? Because it takes energy to get things to go in a direction they don't want to go. So this is actually going to take ATP to drive that pump. So now so far, I haven't actually mentioned aldosterone. Where does aldosterone work? Where we know it works in the principal cell, but what does it do in the cell, exactly? Well, it does three things, OK? So three things. One, let me write it really clearly, is that it drives that sodium potassium pump to work harder. OK. So it basically is going to get even more potassium in the cell and even more sodium over into the blood. So far so good, right? Second thing it does is it puts in little potassium channels here. Well, that's interesting because we know that the cell's got a lot of potassium in it already, right? So if you have a potassium channel, if that's the second thing that aldosterone does, number two, what do you think is going to happen with that potassium in the cell? Where's it going to go? Well, it's going to see that channel, and it's going to say, well, I'm out of here. I'm going to go into that urine. Because there's a lot of potassium in the cell already, and it wants to get over to a place where there's less of it. So it's going to go over to the urine side. So potassium's going to leave the cell. Well, that makes it easier for that pump to work harder because now it's going to squeeze even more potassium into the cell, right? This is going to work even harder to get potassium in there. Because this potassium is leaving and getting into the urine. So, really, at the end of the day, what happens is that the blood-- I'm going to write it over here-- kind of the net effect, the blood is going to, one, it's going to lose potassium, right? Aldosterone is going to make the blood lose potassium. And that makes perfect sense because keep in mind one of the triggers for aldosterone was high potassium. So this is a perfect kind of system to now lower your potassium. It's a nice little loop that you've created, right? More potassium? No problem, make some aldosterone, and aldosterone is going to help you lose some of that potassium. OK, now going back to aldosterone, what's another thing that it does? Well, it does this. It puts in little sodium channels. This is a third thing that it does. Now, if you have a little sodium channel, let's try to think through what would happen. Sodium is going to make its way into this cell, right? Because it's going to say, well, there's not much sodium in there, so I might move into the cell. So sodium gets into the cell. And then again, that sodium potassium pump says, aha, sodium in the cell? , Great, let's pump it into the blood. So it's actually going to move from the cell over into the blood, and that ATP is going to be used up, so it definitely takes energy to do this. But at the end of the day, you're going to move sodium from the urine-- what would have been urine-- to the blood. So another effect, another key effect is gain of sodium in the blood. And think through this. Now if I said at the beginning that the main solute in blood is sodium, right? That's the main way that it's attracting water through osmosis. And now you have more of it, you have more sodium, well, then water is going to also get pulled into the blood, right? It's going to get pulled into the blood as well. And so this is the other key thing that happens. You gain sodium and water. And this is important because, remember, the renin angiotensin aldosterone system, the whole point of it was to raise your blood pressure. Well, now you can see how it actually works because the aldosterone is going to pull in more sodium into the blood, and then water's going to follow, and all of this stuff is going to lead to increased volume or increased stroke volume. And remember, stroke volume relates back to blood pressure. And therefore, blood pressure. So this is how aldosterone works. It allows you to drop your potassium. It allows you to raise your sodium. The sodium pulls in some water, and the water helps you raise your blood pressure because of extra stroke volume. So let's pause right there. We'll pick up with some more stuff that aldosterone does in the next video.