Osmoregulation and Excretion - Online Tutor, Practice Problems & Exam Prep

Osmoregulation and Nitrogenous Waste

Hi. In this lesson, we'll be talking about the excretory system and osmoregulation. Osmoregulation is the homeostatic mechanism that allows organisms to balance their solute concentration and deal with water loss. Now, excretion is the process of eliminating waste from the body and will absolutely involve loss of solutes and water from the body, which is why the excretory system is heavily involved with osmoregulation. But the excretory system has another important job, and that's getting rid of nitrogenous waste, which we'll talk about in just a moment. Now, the excretory system is made up of a few components. The main part is the kidney. That's like the business end of the excretory system. That's this bean-shaped organ; you actually have two, one on either side of your body, and it's going to filter blood plasma and form urine. But its job is so much more sophisticated than that. We'll really get into the details in just a moment. Now the kidney is going to, or the kidney is going to, give off urine that will be transported to the bladder by the ureters. These are going to be tubes basically that lead from the kidneys to the bladder, which is the storage organ for urine. And urine will be stored there until it is ready to be eliminated through the urethra, which is the opening, to the environment. Now, here you can see an example of a fish trying to maintain its osmotic balance, you know, by drinking seawater and, you know, passing water and solutes in and out of its body, and excreting solutes so that it can maintain an osmotic balance in its body. Now, nitrogenous waste is bad because ammonia is a super toxic substance, and it's only safe in the animal body if it's heavily diluted. It's going to form from the breakdown of proteins and nucleic acids. Right? They both have nitrogens in their structures, and those nitrogens are going to be given off as ammonia. This is, for some organisms, okay because they can just heavily dilute the ammonia and eliminate it that way. Here you can actually see what ammonia looks like. It's just a nitrogen with some hydrogens attached to it, and, you know organisms that have plenty of water around them, for example, like tadpoles. They'll, you know, often eliminate their nitrogenous waste as ammonia because water is very plentiful for them. So it's okay for them to waste a lot of water, diluting the ammonia because there's plenty more available. For organisms that have less water available, urea tends to be a better choice in terms of eliminating nitrogenous waste. Now it consumes energy to make urea. Those organisms have to take their ammonia and convert it into urea. And as you can see, ammonia has 1 Nitrogen, urea has 2 nitrogens, and a carbon and an oxygen. It's actually basically formed by combining ammonia and CO2. That's, you know, sort of an oversimplified ve

Osmosis and Osmolarity

Before we get into the nitty-gritty of how the kidney works, I want to review some concepts surrounding osmosis and diffusion. So to start, let's go over a little terminology. A solute is a substance that's dissolved in a solution. And an electrolyte is a specific type of solute that when it dissolves will actually dissociate into ions. So for example, we have salt here. This is just like table salt, and it will dissociate into a sodium ion and a chloride ion in water. Now, when solutes dissolve in water, if they don't spread out evenly, they will form a concentration gradient, which is basically a difference in concentration of a solute over some area. Here you can see we have a high concentration on this side, and a low concentration on this side. There are blue dots representing the solutes. This means that we have a concentration gradient across this area.

Now what's going to happen if we have a concentration gradient and nothing's blocking the movement of these solutes, is we're going to have diffusion, which is the movement of molecules or atoms from an area of high concentration to an area of low concentration. You can see that happening here; this is diffusion, and you can see we have a high concentration here, but these solutes are going to diffuse and spread out evenly throughout the solution.

Now, if we have something blocking those solutes from moving, there won't be any diffusion of solutes. As you can see here, we have a U-shaped tube, and there is a higher concentration of solutes on this particular side and a lower concentration of solutes on this side. But, there's a membrane separating the two sides of the tube. So those solutes won't be able to pass through on either side. They can't diffuse to spread out evenly. But what's going to happen is we're going to have movement of water across that membrane, or osmosis. The water is going to move from the area of low solute concentration to the area of high solute concentration. The result is going to be that the water will balance the solute concentrations on each side. Here, we actually have a higher volume on this side now, but as you can see the concentrations of the two sides here and here are the same. And that is due to osmosis. That membrane is displaying selective permeability. Right? That is the ability of solutes to cross or the prevention of solutes from crossing due to the presence or absence of transport proteins. So here, there are no transport proteins on this membrane for those solutes. So they are not going to be able to cross. It's impermeable to them.

Now, there are terms to describe the concentrations of solutes of 2 solutions. We use the term osmolarity to talk about the concentration of a solute and its measurement of moles of dissolved solute per liter. You don't really need to worry about units for this. I mean, this is biology. You know, we just want to kind of think about it in terms of qualitative terms like something having a higher osmolarity than something else. There are actually specific terms to describe that. So if a solution has a higher osmolarity than another solution, we say that it's hyperosmotic. If the solution that this cell here is sitting in is hyperosmotic, water is going to leave the cell because this area outside the cell has a higher osmolarity, meaning that water is going to want to move out of the cell into that area of higher solute concentration in order to try to balance the solute concentration between the two environments, and it's going to cause the cell to shrivel. So again, the term for that type of solution is hyperosmotic.

Here we have an example of an isoosmotic solution, where the solution outside the cell and the cytosol inside the cell are of the same osmolarity. So the water is going to flow in and out at the same rate. There's no net change in the amount of liquid in the cell. Lastly, the hypoosmotic situation, which you can see here, is going to be when the solute concentration outside, or rather the osmolarity, is lower outside the cell than inside the cell, and so water is going to enter the cell to try to balance those solute concentrations. So again, hyper is higher osmolarity, hypo is lower osmolarity, and iso is the same osmolarity.

Now, there are kind of like 2 osmoregulatory strategies that you'll see organisms have. There are osmoconformers, which tend to be marine organisms that are mostly isoosmotic with their environment. They aren't going to actively regulate their internal osmolarity. Instead, they're just going to let it be isoosmotic with their environment. And that's okay because these are marine organisms, you know, they live in salty water that has a very high solute concentration, which is high enough that it's similar to the concentration inside cells, which is fairly high actually. Now osmoregulators take a more active approach. These are guys who are going to actively regulate the osmolarity of their internal environment. Lastly, I want to mention one really kind of weird strategy that some organisms show called anhydrobiosis, which is a type of cryptobiosis. It's basically an adaptation that allows organisms to survive without any water. These organisms will basically dry out or desiccate, and can still survive for quite some time like that. An example of that is this little guy right here. Its technical name is tardigrade, though I like the common name for it, which is a water bear. And this water bear is all nice and happy and plump with water, but these guys can dry out and shrivel into basically like nothing, and still live like that for quite a long time. So pretty wild adaptation. Lots of organisms have developed different strategies to deal with water balance. So with that, let's flip the page.

Active and Passive Transport

Transport across membranes can be broken down as passive transport and active transport. Passive transport is the movement of molecules or atoms across the membrane via electrochemical gradients. Basically, no ATP is going to be expended to have these molecules or atoms move. They will move due to the natural gradients that exist. Now, a special type of this passive transport is called facilitated diffusion which is essentially a passive transport where these molecules move across the membrane using protein channels or carrier proteins. Protein channels are transmembrane proteins that form a pore through the membrane, allowing specific molecules or ions to pass through. Here you can see we have these 2 different types of molecules, but only these are going to move through the pore because these channels are specific to specific molecules or ions. Now, there's a special type of channel you should be familiar with called an aquaporin and this is a water channel. Water is a small enough molecule that it can diffuse through the membrane without any assistance. However, it doesn't diffuse through at the rate necessary to sustain living processes. So organisms use aquaporins to make the passage of water through membranes much more efficient. It's actually amazing how much more efficient it is if you look at the numbers. Now, carrier proteins are a little different than channel proteins. Channel proteins are just like a hole that things can go through to get through the membrane. Carrier proteins have to actually carry a molecule through the membrane. So they'll actually bind a molecule on one side, and then they'll change shape. In that process, they'll actually carry the molecule through the membrane and eject it on the other side. It's not like a pore. It's different. It's almost like, you know, a train moving through a tunnel or something. Right? Like the molecule has to board a car and then it moves through the membrane and then it's released. Now, active transport, unlike passive transport, consumes ATP directly in order to move molecules or ions across the membrane. Now, there are 2 types of active transport that we classify as primary active transport and secondary active transport. Primary active transport directly hydrolyzes ATP to power protein pumps. The most famous example of these pumps is the sodium-potassium pump that is used for everything. It's everywhere in the body. It's probably the most important pump for you to know. Sometimes it's called Na_K ATPase, which is an abbreviated name for it. Now, what this sodium-potassium pump is going to do is move 3 sodium ions and 2 potassium ions in opposite directions across the membrane. Here, you can see Na_K ATPase in action. What we have is, these are our sodium ions and they're going to get loaded up in here. The 3 of them are going to get ejected on the other side, and that is going to require some ATP hydrolysis. These potassium ions will get loaded up in here. This phosphate group will be ejected causing a conformational change that releases these 2 sodium ions on the other side. You don't need to know the specifics of it. I just go through it because, you know, it's interesting and it can't hurt to know these things. Now, cotransporters are going to be a type of secondary active transports. Secondary active transport is going to harness the potential energy created by pumps. So it doesn't itself consume ATP in order to move things, but it uses the concentration gradients set up by pumps that do consume ATP in order to move substances across the membrane. Now, if you're thinking, well, how is this any different from passive transport if they're just both using gradients? The difference is in secondary active transport, those gradients have to be actively maintained by pumps. If you shut the pumps off, you would lose secondary active transport as well because they rely on the gradients built by those pumps. So, in a sense, they're indirectly using the ATP as well. Now, cotransporters are going to carry out secondary active transport using their gradient, and they're going to use the energy from that to carry another substance against its gradient. And this can work in two directions actually. Let me jump out of the way here. So you can have simporters, which are going to move both substances in the same direction. So here, we have a symporter. It's going to take 2 things, move 1 along its gradient and the other against its gradient. But moving one thing along its gradient will provide the energy to carry the other molecule or atom through. Now, antiporters are very similar in concept. The only difference is they are going to move the substances in opposite directions across the membrane, but it's the same idea. One substance moving along its gradient is going to power the movement of another substance against its gradient.

Kidney and Nephron

Kidneys are the major organs of the excretory system, and they're heavily involved in osmoregulation. They actually have two layers. This outer layer we call the cortex and an inner layer known as the medulla. And it's this inner layer that's going to be the saltiest layer. And the kidney is basically mostly made up of these functional units called nephrons. And these are tube structures that transport filtrate, which we'll talk about more in a moment. And these tube structures are going to be surrounded by blood vessels. Now nephrons are going to use the active transport of solutes to create salty environments that will help these nephrons and the kidneys reabsorb lots of water from the filtrate. And as I said, there are two layers to the kidney. You have the cortex, which is the outer layer, and the medulla, which is the inner layer. And you actually will see two types of nephrons in kidneys. You'll have what are called cortical nephrons, like cortex, and these are the most common type of nephron. And basically, the tubules of these nephrons just don't extend that deeply into the medulla. See, here's the boundary between the cortex and the medulla, here is a nephron. Jump out of the way. And you can see that this nephron only extends a little bit into the medulla, whereas this other nephron is a juxtamedullary nephron, which is mostly responsible for maintaining that osmotic gradient for reabsorption. So, the cortical nephrons are there to filter the filtrate and create urine and reabsorb lots of stuff. The juxtamedullary nephrons are not as common because their job is more of a support role. They're just there to make sure that this area stays super salty, and that's why they extend very deeply into the medulla as opposed to the shallow extension of the cortical nephrons. And, hopefully, you can see in this image that we're basically over here, we're looking at like a slice of this. It almost as if you took, you know, a chunk out like that and zoomed in, that's what you'd see. And hopefully you can also see just how riddled with blood vessels the kidney is. It's super infused with blood vessels, and you'll see why momentarily this is so important. So with that, let's actually go ahead and flip the page.

Filtration, Reabsorption, and Excretion

We're going to break down what happens in the nephron into 4 categories. The first is filtration, and that's when water and small solutes will cross the epithelial membrane and form filtrate. This is going to happen in a structure called the renal corpuscle, which is made of these two parts you see here, the glomerulus, or glomerular capillaries, and Bowman's capsule. Basically, the fluid in the blood is going to cross over from the glomerulus into Bowman's capsule and be filtered and form filtrate. When the liquid enters Bowman's capsule, it is then considered filtrate, which is just a solution of water and small solutes like salts, sugars, and amino acids, as well as nitrogenous waste. What you don't want to find in filtrate is big stuff like proteins or even cells. That means the kidneys are damaged, and that's really bad news. You know, you must get that taken care of right away. The point here, though, is that filtrate formation is not very selective. Lots of water and solutes will make it through to the filtrate.

But that brings us to reabsorption, which is the most important thing the nephron does. Valuable solutes like glucose and vitamins will get actively reabsorbed from the filtrate into the blood. In addition, salts will be reabsorbed, and water will move passively by osmosis to follow those solutes that are actively maintained. Reabsorption is highly selective and tightly regulated. Hence, while filtrate formation is not selective—everything is going to get dumped into the filtrate—only important and beneficial substances for the body will get reabsorbed back from the filtrate. This mechamism cleanses the fluids of the body because everything is pushed out into this contained area, and then you selectively reabsorb the substances you want. This way, you can also get rid of toxic substances, like nitrogenous wastes.

Now, you have secretions. Some wastes and solutes will actually be actively added back into the filtrate from the blood. Similar to the specificity of reabsorption, secretion allows the body to specifically rid itself of certain things, which not only gets rid of toxins but also helps the body maintain proper osmotic balance. At the end of the day, you're going to excrete this filtrate after everything has been reabsorbed and various things have been secreted into it. You can see these individuals here doing a pee dance because they have to excrete it. Basically, at the end of the day, excretion is going to equal what you get from filtration, plus what you get from secretion, minus what is reabsorbed. So, what's actually excreted at the end of the day is going to be only a small amount of what goes through filtration, because a lot of that is going to be reabsorbed. And here you can see how those different components are broken down throughout the nephron. This is a very simplified version of the nephron.

And with that, let's actually go ahead and flip the page.

Glomerulus and Bowman's Capsule

All of the fluid that's delivered to the nephron comes from blood vessels, which is why there are so many blood vessels that proliferate the kidneys. Now specifically, the nephron is going to have what are called these peritubular capillaries that will surround them and specifically surround the portions known as the proximal and distal tubules. Now the portion of these peritubular capillaries that surrounds what's called the loop of Henle, is known as the vasa recta. And here, in our image of the nephron, let me jump out of the way, you can see our vasa recta here, those red tubes surrounding the loop of the nephron, or loop of Henle, this yellow U-shaped structure here. And then up here, we have our peritubular capillaries that are surrounding the proximal, and over here the distal tubules. The point being that the kidney's job is to filter the fluid in the blood, and so there must be a lot of blood that makes it to the kidneys in order for it to be able to filter that. That's why there are so many blood vessels in the kidneys and surrounding the nephrons. Now the beginning of the nephron, because it is easier to think about these as like a linear path, even though they are actually just tubes that are all wound up around each other, we're going to think of it as a linear path. And the beginning is the renal corpuscle, which you can see right here. This is our renal corpuscle. It's made of 2 components, the glomerulus, which is, I'm just going to write glom. This ball of capillaries here, that's our glomerulus, and that's going to provide the blood to be filtered. You can also see the glomerulus right here, but I don't think it does it justice because, you know, really it's a ton of capillaries in there. Now, surrounding the glomerulus is Bowman's capsule. This structure that you see here that is, Bowman's capsule. And its job is to collect the filtrate as it flows out of the blood. So the filtrate is going to go from the glomerulus into Bowman's capsule. And filtration occurs, you know, due to the blood pressure actually that will drive fluid into Bowman's capsule. It's literally the pressure from the heart that drives this process. And the renal corpuscle is going to kind of act like a sieve, you know, like a strainer for pasta or something. It's going to filter stuff based on size. So big molecules or cells, will not be allowed through, only small solutes and water. In fact, if you see big molecules or cells, that can indicate damage to the renal corpuscle, and that's bad news. Now because so much stuff makes it through this sieve, this filter, a lot has to be reabsorbed. Right? A ton of fluid is lost to the filtrate initially, but about 99% of the filtrate is going to be reabsorbed before it's excreted. So it's going to minimize water loss, but it's also going to allow for selective reabsorption. That's why the kidneys act really as a filter system for the body because they push a ton of fluid through these tubes and then only reabsorb the good stuff that they need. So with that, let's flip the page.

Proximal Tubule

After the filtrate is collected in Bowman's capsule, it's going to move into the proximal tubules. So here you can see the glomerulus filtrate is going to move this way. And the proximal tubule has what's called a convoluted structure. Basically, it's like a spaghetti noodle all wrapped up, lots of twists and turns, and, you know, coils in order to maximize the amount of area it provides while minimizing the amount of volume it takes up. You know, a common tactic in biology. Now it's going to transport filtrate from Bowman's capsule to the loop of Henle. Because it is involved in reabsorption, it has that convoluted structure, and it also has microvilli in the lumen, which both of which are going to greatly expand the surface area of the proximal tubule, which is important for reabsorption. Right? So glucose, amino acids, salts, and other solutes are going to be reabsorbed by active transport. You can actually see a whole list of the stuff that's going to be reabsorbed right here. It's a ton of stuff, and water is going to passively follow those solutes. Because both solutes and water are reabsorbed together, the osmolarity of the filtrate is not going to change from reabsorption in the proximal convoluted tubule. So the total volume will decrease because a ton of stuff's going to get reabsorbed, but the osmolarity will stay the same. And, here in this figure behind my head, you can see other areas of the nephron and what they will be reabsorbing. Here, you can see some stuff that will actually be secreted into the proximal convoluted tubule. Those are secretions. Next, we're going to move on to the loop of Henle, which is this structure here. And then we'll make it to the distal convoluted tubule here, and finally to the collecting duct. And you can see that all of these structures are specialized for the reabsorption or secretion of various materials. So with that, let's flip the page.

Loop of Henle

The loop of Henle is a massively important structure of the nephron that not only absorbs a lot of water and salt, but also plays an important role in maintaining the osmotic gradients of the kidney that are necessary for water and salt reabsorption. Now the loop of Henle connects the proximal tubule to the distal tubule, and it goes in and out of the medulla. It dips its loop into the medulla and then comes back out. And remember, depending on the depth to which the loop of Henle enters the medulla, you would classify a nephron as either a cortical or a juxtamedullary nephron. The first part of the loop of Henle, the one that goes into the medulla and connects to the proximal convoluted tubule, is known as the descending limb. This is a thin portion and it's permeable to water, and lots of water reabsorption occurs here. This is going to cause the volume of the filtrate to decrease because it is losing lots of water. However, it is not reabsorbing any salt. Only water is being reabsorbed here. That means that the solute concentration of the filtrate is going to increase. So it's actually going to become a more concentrated filtrate.

The ascending limb has a thin section and a thick section. Basically, in the nephron, thin sections do not do active transport, while thick sections do active transport. That is the difference. You need a thicker tubule to attach all those pumps, and specialized structures to actively transport molecules, whereas, you want a thin structure when you're mostly going to rely on passive transport because the distance that something has to travel will affect its rate of diffusion.

So the ascending limb starts off with passive transport in the thin section, and it's going to be reabsorbing salt, and it is impermeable to water, and then the thick section will actively reabsorb salt, and the whole ascending limb is impermeable to water. So only solutes will be reabsorbed. Here, because solutes are being reabsorbed but water is not, the volume won't change. The volume is going to stay the same. But we are diluting the filtrate because we are taking solutes out. So the filtrate is concentrated in the descending limb, and then diluted in the ascending limb, because we are absorbing water on one side and salt on the other.

This actually is a special type of countercurrent exchange we call a countercurrent multiplier system, which is basically a system that expends energy to create a strong concentration gradient that it's going to use for countercurrent exchange. The way this happens is the deeper you get into the medulla, the saltier it is. Water will flow out of the descending limb due to the osmotic gradient created by the ascending limb. So this portion of the loop of Henle creates the gradient necessary to reabsorb water on this side. That's the countercurrent aspect to this.

Because, just something to consider is that as the filtrate moves down the loop of Henle, it gets more and more concentrated, right? Because it's going to lose water along the way, as water is going to be reabsorbed. But as the filtrate gets more and more concentrated, so does the osmotic gradient outside the loop of Henle. You know, that’s the other aspect of this countercurrent system is that as it requires a greater and greater osmolarity to reabsorb the water, the medulla provides a saltier and saltier environment to accomplish that. So basically, high solute concentrations at the beginning of the ascending limb are what are going to drive solute transport. Because by the time the filtrate makes it here, it's going to be so super concentrated that when it moves into the ascending limb, where it's no longer permeable to water and now permeable to solutes, the filtrate is going to be more concentrated than the environment outside of it, and so it's going to reabsorb salt. Salt is going to move out of the filtrate into this super salty environment, and that's going to dilute the filtrate as it moves up the ascending limb. However, when it reaches the thick portion, the filtrate is too dilute to be moved based on those osmotic gradients anymore, and that's why active transport is used in the last portion, in order to keep reabsorbing salt and maintain those osmotic gradients, despite no longer being able to rely on passive transport. And finally, after that long journey up and down the loop of Henle, filtrate's going to make it to the distal convoluted tubule, which is almost the end of its journey.

Distal Tubule and Collecting Duct

The distal convoluted tubule connects the loop of Henle to the collecting duct, and it's going to actively reabsorb solutes and can also reabsorb water. The collecting duct is the final tubule element, and it can reabsorb water and urea. In fact, the region in the inner medulla of the collecting duct is permeable to urea, which helps to create that strong osmotic gradient inside the medulla. So just another way that the nephron uses, you know, simple concentration gradients in order to maintain osmotic balances and help drive the whole process. Here you can see another diagram, which shows how the nephron is structured and what gets reabsorbed where. I've basically tried to provide many different images, that all kind of show the same thing more or less so that hopefully one of them is one that you really like and is going to be one that you want to refer back to. It's the reason I'm providing all these different images, even though a lot of the information is redundant. It's just to give you an option of a diagram to refer to. Now, the filtrate that makes it through the collecting duct is ultimately going to be excreted as urine. But before that happens, there's going to be some hormonal regulation that's going to affect the distal convoluted tubule and the collecting duct. We're actually going to talk about two hormonal systems here. The first is antidiuretic hormone, which is sometimes called ADH or vasopressin. Now, I'm just going to call it ADH. ADH is a hormone secreted by the pituitary gland in response to high blood osmolarity, meaning, like, high solute concentration in the blood. What it's going to do is cause the walls of the distal tubule and the collecting duct to become more permeable to water. And it does this by adding aquaporins to the apical membrane. So here you can see a small model of that happening. I don't want you to worry about the details here. All I want you to notice is that we have ADH, which is a hormone that's going to move through the bloodstream, bind to a receptor on a collecting duct cell, and that's going to cause more aquaporins, to be integrated into the membrane to allow for more transport of water. And this is ultimately going to lead to a large increase in water reabsorption right before it's lost as urine. Right? This is sort of like the last place that we can really do reabsorption. And that water reabsorption is going to lead to an increase in blood volume, but because we're only reabsorbing water, or we're only increasing the reabsorption of water and not increasing the reabsorption of solutes, we're actually going to decrease our blood osmolarity. So that's why this is secreted in response to high blood osmolarity to lower the blood osmolarity. And it also will help increase the blood volume. So this will also be a mechanism involved in maintaining blood pressure. You can see that it can get quite complicated. I don't want you to try to memorize this chart. Really, I'm just putting it here to illustrate how complex and interconnected the maintenance of this system is. So with that, let's flip the page and talk about our last hormonal system involved with the kidney.

Renin-Angiotensin-Aldosterone-System

Okay, everyone. In this lesson, we are going to be talking about the Renin Angiotensin Aldosterone System that is utilized to regulate your blood pressure and your blood volume. Okay. So the Renin Angiotensin Aldosterone System has an incredibly long name, so we usually don't call it by that name. We usually call it the RAS system, or simply RAS. And like I said, it's going to control your blood volume, and it's going to do this by increasing your salt and water reabsorption inside of your kidneys. But it's not that simple. Based on its name, you guys can tell it has a lot of components, and it's going to have many different hormones that work together to raise that blood pressure and that blood volume. Now the loss of blood pressure or blood volume could be caused by many things. It could be caused by severe dehydration where you don't have enough water in your blood. It could be caused by blood loss, something like that. You need to make more blood. You need to have more water in your blood. This system is going to help you do that.

So, the very first cells we're going to talk about are going to be these juxtaglomerular cells in the Juxtaglomerular Apparatus. That word is always hard for me to say. So these Juxtaglomerular cells are found in the juxtaglomerular apparatus. And from now on, I'm simply going to call them JG cells because that is a common shortened version of their name since it is kind of difficult to say. And these JG cells are going to be found in the kidney. But specifically, they're going to be found in the blood vessels of the kidney. And what these cells are going to recognize is they're going to recognize whenever the blood pressure or the blood volume drops. So they're going to recognize when the blood volume actually drops, and they're going to release this protein called renin. Renin is going to be the beginning of this entire process. Renin is going to be made by these JG cells inside of the kidneys, and then renin is going to go on and start signaling all of these other hormones to begin.

So it says here that renin leads to the cleavage of Angiotensin to Angiotensin 2. And actually, it's not that simple. There's Angiotensin, but it can also be called Angiotensinogen. It's just a longer name for the same thing. And what's going to happen, I'll draw it down here, Angiotensinogen is going to interact with renin. So these two are going to interact. Now, renin is made by the kidney cells, those JG cells. And angiotensinogen is going to be made by your liver cells. But angiotensinogen can't do anything in the form that it's in. But once it reacts with renin it's going to be transformed into Angiotensin 1. Angiotensin 1 is going to be an active form of this Angiotensin hormone. Angiotensinogen isn't active until it interacts with renin. And what renin's going to do is it's going to cut part of the angiotensinogen molecule off and create Angiotensin1. And then, Angiotensin 1 flows through the blood vessels, and it's going to be converted to Angiotensin 2. This is going to be the one I want you guys to remember because it's going to do a whole bunch of really interesting things. So how is Angiotensin 2 actually made? Angiotensin 2 is going to be made by these very specific enzymes called angiotensin converting enzymes or ACE. So ACE is going to do this to Angiotensin 1, and it's going to change it to Angiotensin 2. That is going to be the magical form.

Angiotensin 2 raises blood pressure by vasoconstriction, and it's also going to stimulate the adrenal cortex to release aldosterone. Now, Angiotensin 2 can also directly affect the kidneys and tell the kidneys to reabsorb more water, and it can also tell the Pituitary Gland to secrete ADH, the antidiuretic hormone, which is also going to make you reabsorb more water inside your kidneys.

Okay. So, angiotensin 2 is going to tell the Adrenal Cortex to create Aldosterone. Aldosterone does some interesting things. Aldosterone is going to stimulate the distal tubules and the collecting duct of the kidney to reabsorb more salt. And you may be thinking, well, to increase blood volume, we don't want salt, we want water. But remember, the process of osmosis, water is going to flow towards the area of higher solute concentration. So if inside of your body has a higher solute concentration, you are going to reabsorb more of that water from your urine, and you're not going to release as much water. So this is actually a good thing. So the ADH, antidiuretic hormone, is going to make you reabsorb more water. The aldosterone hormone is going to make you reabsorb more salts, which will inevitably also make you reabsorb more water.

So as you guys can see here, it says water follows the reabsorption of salt, leading to the increase of blood volume and blood pressure. That is great. So, let me just make a little arrow so you guys know that I was talking about that down there. So this is going to increase the blood volume, but you may be thinking, oh, it's going to increase the salinity of the blood as well. It's actually not because Aldosterone also causes that water to come in. So it's not too salty or anything like that. Now, I also want you guys to know that this whole system can be triggered by the sympathetic nervous system as well. In case there's an emergency if you go into a fight or flight syndrome or response, you will also stimulate this particular pathway, but you're going to stimulate it through a different means, and it's going to be the pituitary hormone, ACTH, and it's going to stimulate the production of aldosterone, which is going to increase your blood pressure. And you may be thinking, why do you want high blood pressure whenever you're in a fight or flight system? Well, you want this because it allows all of your organs to get all of the blood that they need because it's increasing blood volume. It's ensuring that all of your organs, your muscles, your lungs that help you get away from the threat have the blood supply that they need. So you need to reabsorb as much water as possible to create that perfect high blood volume and blood pressure.

But the majority of the time, we are going to use the renin angiotensin aldosterone system, or RAS, for whenever we have low blood volume; I think that that is really helpful. This is basically just diagramming all of the stuff I just told you. Okay? Alright. So it doesn't fit all perfectly. I will get out of the way in a second. The only thing that's really being cut off is going to be the lungs and the top word up there, but I will explain that. So let me scroll up a bit so you guys can see everything. Okay. So where does this whole process start? Remember, the whole process is going to start whenever those kidneys realize that the blood volume is not high enough. So that's going to be right here. The decrease in renal perfusion, or there's not enough blood in the kidneys, is going to cause those JG cells to realize that there's low blood volume, and they're going to create renin. So this is going to be the very first step. So they're going to create renin, and then it's going to go this way. Okay, everyone? So what does renin do after that? Remember, after this, renin is going to interact with the angiotensinogen hormone that is made by the liver. And once it interacts with the Angiotensinogen hormone, it's going to create Angiotensin 1. And this is the second step in the pathway. And then the ACE enzyme is going to turn Angiotensin 1 into Angiotensin 2. And here's the ACE Enzyme up here. So now we have Angiotensin 2, and this is going to be th