All right, ninja nerds. In this video, we're going to take a nice brief overview of everything that we've covered throughout the series of videos in the renal playlist. So, if you guys have already watched it about the proximal convoluted tubule, you guys have watched the glomeal filtration process, the loop of henley, the distal convoluted tubule, and the collecting duct videos, then what we're going to do is we're going to take a nice little brief overview over that just to make sure that we got all of this stuff clear. All right, so let's go ahead and start that. So if you guys remember what did we say was happening? Well, we said that this was the aair material, right? Coming in to the actual glomemeulus. And the glomemeis was that set of capillaries that was the filtering structure, right? And what did we say here was happening? Well, we said there was a mixture of pressures, right? The pressures that was trying to push out was the glomemeular hydrostatic pressure which was inside of the capillaries exerted by what? The blood pressure, the systemic blood pressure. Then what else did we say? We also said that there was an osmotic pressure of the uh specifically the proteins with inside of the actual blood that were trying to pull water into the bloodstream. Then we said that there was a capsular hydrostatic pressure that was actually going to be due to the filtrate trying to drain. Sometimes some of that filtrate can back up and exert a pressure trying to push certain filtrate back into the actual glomeilus. That was called the capsular hydrostatic pressure. And then we said that there was a capsular osmotic pressure but it should be zero because there should be no proteins plasma proteins like albumin that should be filtered across this membrane because if you remember the capsular osmotic pressure was trying to pull fluid out into the glandular space. All right. So now that we know all of those again we remember what was the overall outcome of this. We said that there should be a net filtration pressure of approximately 10 millm of mercury. Right? We said that that's what it should be. The net filtration pressure should be approximately about 10 mm of mercury. What else do we say? Remember that relationship we uh made with net filtration pressure. We said the net filtration pressure was directly proportional to the glomemeular filtration rate and we said that the glamular filtration rate should approximately be about 125 milliliters per minute. We did that calculation in the glomemeular filtration video. So that is our GFR. The glomemeular filtration rate which is directly proportional to the net filtration pressure is how much fluid in volume per time is being filtered across this actual glomemeular filtration membrane. And we said a lot of different fluids were being passed across this membrane. Right? Before we do that though, what was this actual arterial here supplying the glomemeilus? If you guys remember, this was the aerant arterial. Right? And we said that this was one of the weird examples of the body that in a capillary bed was actually fed by an arterial and then drained by an arterial. So this is an example of a eerant arterial because this is actually draining the actual capillary bed. Then what do we say? This filtration process occurs across the membrane. A lot of fluid and a lot of different different types of filtrate substances are actually going to be accumulated across this area and drained into this next structure here. What is this next structure here? We said that this is the proximal convoluted tubule. And this is one of the more important sites of the actual nephron. What is a nephron? If you guys remember, we said a nephron was the glomemeular capillaries plus the bowman's capsule, right? Which is made up of the visceral layer, which is the pottoytes and the parietal layer, which was made up of those simple squamos epithelial cells that made up the renal core pusle plus the proximal convoluted tubule, the loop of henley and the distal convoluted tubial. that was an efron and we have about 1.2 million in one kidney. So if we have two of them generally unless you have renal aenesis unilateral generally you're going to have two kidneys and it's going to be about 2.4 4 million, right? So that's pretty cool. Anyway, we get to the proximal convoluted tub. What do we say happens in this area? A lot of reabsorption, a lot. Let's start with that first and then we'll talk about the secretion mechanisms. So we said a lot of sodium was reabsorbed here. We said a lot of water was reabsorbed here. We said a lot of potassium was reabsorbed here. A lot of chloride. A lot of magnesium. Um, decent amount of calcium is reabsorbed here. And what else did we say was reabsorbed here? Bicarbonate. So exactly about how much of these guys and there was more. We'll mention a couple other ones, right? But sodium about 65% of the actual sodium is reabsorbed. And what did we say was really important about that? We said that because 65% of the sodium is being reabsorbed, water feels obliged to follow. And we said that that would be approximately about 65%. We said by carb generally depending upon the body's demands generally about 90% of the by carb is reabsorbed about 85 to 90%. Magnesium it's kind of questionable. Certain literature will say different. We're just going to say it's questionable the amounts of magnesium that are going to be reabsorbed. Potassium is around the range of about 60%. Okay, around the range of about 60%. And chloride ranges to about 50 to 60% also. All right, calcium about 60% of the calcium is reabsorbed here. We said, right, 60% of the calcium is reabsorbed here. A lot of different things reabsorbed here. And again, what is the definition of tubular reabsorption? We said tubular reabsorption is defined as the process in which substances from the actual kidney tubules, this filtrate is moving where? We said that these substances are moving from the actual kidney tubules where into the blood. All right. from the kidney tubules and into the blood. So if this sodium is moving this area, this water is moving to this area, this bicarb is moving to this area and the magnesium and the potassium and they're going into the blood. This is defined as tubular reabsorption. We talked about many of the mechanisms how sodium is brought in, how water, how by carb we're not going to do that. We don't need to, right? But one thing I do want to mention is what actually is brought in with sodium and what is also going to be another process we'll talk about just a second. Remember glucose, one of the organic nutrients and amino acids, amino acids, these substances did what? Remember they actually went with sodium by the sodium glucose and sodium amino acid co-ansport mechanisms. Those were also important. So glucose and amino acids were also reabsorbed in this process dependent upon the actual presence of sodium. We said what else did we say gets reabsorbed? small amounts of ura gets reabsorbed. Let's use this actual green color for ura. So ura about 50% about 50% of the ura is actually going to get reabsorbed into the body right back into the bloodstream. Oh good question. How much of the glucose and amino acids physiologically should be 100%. If you have traces of glucose in the area and they call that glucose, right? And usually glucose ura is identifiable by someone who's actually having diabetes. So it's not normal to have glucose in the air because 100% of that should be actually being reabsorbed. And the reason why is we have these transporters here that are designed to be able to bring in the sodium and the glucose. And they can bring that up until the blood levels usually the actual glucose levels in the bloodstream go above 180 milligrams per dl. Then the transporters start getting saturated and you you reach what's called the transport maximum and then it starts getting lost in the urine. Okay, so we talked about that. What other things were being reabsorbed here? Not just ura and all these different electrolytes. We also said that small proteins were being absorbed here too. So small molecular weight proteins, small proteins like insulin, albumin, we said even a little bit of the hemoglobin, these molecules could actually get reabsorbed. So small proteins can actually get reabsorbed into the bloodstream. And we said it was by an endoccytosis mechanism. What else did we say? We also said that lipids, remember lipids, they they're really weird. Lipids actually get reabsorbed in this process too because what? It's passive diffusion. They can diffuse right through the phosphoipid billayer. So the lipids can also get reabsorbed into the bloodstream. Okay, so we talked about lipids, small proteins, all of these different electrolytes and the organic nutrients. What else? And then even this metabolic waste ura. What about the things that are being secreted? How we define tubular secretion? It's the process of moving things from the blood into the actual filtrate. How does that happen? Well, you know that we can actually excrete certain drugs in this area. So, we can actually take certain drugs. We're not going to go over the many drugs that you can actually excrete in this process, but one thing I do want you guys to know is that in order for us to excrete drugs in order for us to excrete protons, in order for us to excrete other different types of metabolic waste products. So, other different types of metabolic waste products. For example, ammonium and even small trace amounts of creatin uh creatinine. These substances here, in order for them to get pumped over here, it depends upon the presence of ATP. We need ATP in order for us to be able to pump these substances from the blood and into the actual filtrate. So all of these processes here require the presence of ATP. Okay, now that's one thing. And not only can you actually uh push these protons out, right? Depending upon what the situation might be, if you're in a situation when you're in metabolic acidosis, you'll pump the protons out, you can also get rid of by carb. So there is certain situations in which you can actually lose by carb, but we'll talk about that when we get over to the intercolated B cells. Okay, so for the most part, this covers in general what we talked about in the proximal convoluted tubial video. Then as we get down to the loop of Henley, what did we say? Actually before we do that, what was the milliosmos? We got to make sure we bring up that milliosmal concept, right? The osmolality. What do we say was the general flow as we move our way down? Okay, we said as we move our way down, it goes from about what? It goes from 300 millosm moles and it works its way downward from that point. Let's see how that goes. Okay, so if you guys remember, it starts up here at 300 millosmals. Then it works downwards to about 500 millosmals. Then we get down to about maybe 700 millosmals. Then we get down to about 900 millosmals. And then as we get really really deep down into the renal medulla, it can hit 1,200 millosmals. Now really, really briefly, let me show you what I'm talking about here in a side diagram. Let's come over here for a second. Just a real quick side diagram. I'll draw a kidney here so that we're clear. Let's say I take one piece here. I take one lobe here. Okay? And here's a kaix which is going to collect the actual urine that's dripping off. This is a renal pyramid. The renal pyramid is two parts. This part here is the cortex. It's more of like the lighter granulated tissue. And then the other part was the renal medulla. And that was that nice little striated part, right? And that was due to a lot of the kidney tubules. Now what we're trying to say here with this renal you know medularary gradient is that as you move your way from the cortex which is where the proximal convoluted tubule and the uh distal convoluted tubule and even the glam capillaries at we move down 300 500 700 900 1200 that's what we're saying. So the actual osmolality or the medularary gradient is increasing as you go down that's what we're trying to say. Okay, so now that we got that, let's come back over here for a second. Okay, so what did we say was the plasma osmolality of the actual the blood the blood plasma? We said it was approximately around 300 millosmals. And then we said due to the filtration process as it's moving across we said it should be equal. So isotonic, right? So this actual should be 300 millosmals in the proximal convolute tubule. These should equalize. So they should be isotonic with one another. Then we said after all the reabsorptive and secretion mechanisms when it comes out here into this descending limb it should be what? 300 millosmals. Let's do this in a different color. Let's make it bright so that you guys remember. Let's do with this color here. Oo, let's do it with orange. Let's make this 300 millos. So whenever it's leaving when it's leaving the proximal convoluted tub, it's 300 millosmles. Okay, sweet. Let's get back to this. As we go up the ascending limb of the loop of Henley, what did we say we had there? Remember, we were pumping in from the filtrate. We were pumping out sodium, we were pumping out potassium, and we were pumping out the two chloride ions, right? Through the sodium potassium 2 chloride coransporter. And this was happening along the entire length of the ascending limb. And it was doing a lot of this, right? How much of this sodium, this potassium, and this chloride is actually getting pumped out? Well, it's a decent amount. Not as much as in the proximal convoluted tubial, but it's still a decent amount. Remember, we said about 65% of the sodium here, and it's about 25% of the sodium within the ascending limb. For the potassium, it honestly, it ranges. So, generally, they say it's approximately about 30%. And then for the chloride ions, this is about 30%. Okay, so again, sodium 25%, potassium 30, and chloride about 30%. What about the calcium and the magnesium? Remember we were actually having what was happening? Remember some of those potassium ions? Where's my green marker? There it is. Remember the potassium ions? Some of the potassium ions were leaking back in because of the different gradients, right? And then when the potassium was leaking back into this actual tubial lumen, it was generating a nice positively charged membrane depolarization, right? And what did that do? It caused some of those calcium ions that was in this area to leak out. Remember there was calcium and there was magnesium and these ions started leaking out by that passive parasellular transport right out into the actual meillary space and they were also contributing to the meillary interstitial gradient making it saltier as you go down. So what did we say? We said if we had a lot of sodium, a lot of potassium, a lot of chloride, a lot of magnesium, and a lot of calcium that was making the medulla really salty. And then what do we say? We said here that water's coming down. He's like, a lot of saltiness over there. I got to go. So what happens? A lot of the water starts leaking out through the aquaporn once into the medularary interstitial space to where there's actual all these solutes particularly sodium and chloride. Right now when that happens when a lot of this water is leaking out due to the sodium and the potassium and the chlorides and the calcium and the magnesium getting pumped out as it's going up what did we call that? We called that the counter current multiplier mechanism, right? Okay. Sweet deal. So that was where a lot of the water is getting reabsorbed. So a lot of the water is getting reabsorbed right here too. So we said 65% there. It's approximately about 25% here. Okay. Because right with 65 plus 25 65 plus 25 is zero. Carry that one right there. Yeah. So, we're good. Yeah. Sorry. So, again, about 25% of the water is reabsorbed right here. Reason why I did that is because there should only be about 10% left whenever we get up to the actual uh specifically the distal convoluted tubule. Okay. Okay. 25% of the water. We got all that part there. Now, as we take this guy up. Okay. As we take this guy up, we're going to bring this actually should not be 25%. This should actually be 15%. I'm sorry. Let me fix that. This should be 20% water left over. Okay. So, as we bring this actual filtrate up, what do we say? Okay. Well, we're going to look at the actual tenicity for this in order for us to understand this. We lost a lot of water. As we lost a lot of water out of the descending limb, what are we losing then? Remember that the concept of tenicity? We said there was hypertonic and then we said that there was isotonic and then we said that there was hypotonic. Hyper means that there's more solute less water. Isotonic means that there's just an equal amount of water and solute. Hypotonic means that there's actually a lot of water and less solute. Well, we lost a lot of water. If we lost a lot of water, that means that this is actually going to be hypertonic as compared to the plasma osmolality. So, right here it should be hypertonic. Okay, queen. So, hypertonic right there. As we make the turn and we go up, then what are we doing? We're pumping out a lot of salt, potassium, chloride, calcium, magnesium, and there's still about 20% of the water left over. If that's the case, then as all this process is occurring throughout the entire length of the ascending limb, by the time we go into the distal convoluted tubial, what should it be? It should be about 100 to 200 millos moles. So this is very hypotonic, right? A lot of water, very little solute. It's not very salty. And this is why that's why I made that little mistake. Sorry. 20% of it should actually be water. And then a little bit of it, about 10% of it should actually be sodium. Okay. All right. Cool. So hypertonic. As you get done with this one, this should be hypotonic. Then as we went into the distal convoluted tubial said there was two parts, the early distal tubial and the late distal tubial. If you guys remember, we kind of separated those kind of like right here, right? And what did we say happened? We said within the early distal tubule, we had those sodium and chloride simorters, right? We were bringing the sodium in and we were also bringing the chloride in. And we were doing it through these actual nice protein channels. But the only way that we could really do this was on the basolateral membrane. What did we have? We had those sodium potassium pumps which were constantly pumping the sodium right against its concentration gradient and the potassium against its concentration gradient. Approximately three sodium for every two potassium. And what do we say this process required? It required a lot of energy. So it required ATP. But it helped to be able to do what? It helped to be able to bring the sodium and the chloride in. And then what could happen with these guys? We said that the sodium could actually be brought out into the blood and the chloride could be brought out into the blood. Right? And this is a process of reabsorption. Okay. What else did we say could happen here? We also said that at the other early part of the distal tubule, there's specialized uh specificity depending upon hormones, right? Remember there was that hormone that we talked about produced by a gland. Let's actually show that up here. Remember we had here the thyroid gland and then on the back of the thyroid gland you had these tiny little glands here. They were called the parathyroid gland and they were producing a special hormone and that special hormone was called the parathyroid hormone. And what was the parathyroid hormone responding to? It was responding to low blood calcium levels hypocalcemia. So whenever there is hypo calcia this can be a stimulus to the parathyroid gland and cause the parathyroid hormone to produce to be produced and again what is hypocalcemia low blood calcium levels when the parathyroid hormone comes over here what did he do remember he stimulated a groin coupled receptor and the overall result was he activated cyclic AMP we're not going to go through the whole mechanism here but remember he activated cy cyclic AMP which activated protein kynise A and what did that do that activated a specialized channel and this channel is is a modulated channel right it's dependent upon parathyroid hormone so what protein kynise A does is he comes over here and phosphorolates that channel and what happens it allows for calcium that are still in the filtrate right because about 10% of the calcium is actually going to be coming about to this point here the calcium can get reabsorbed here but it depends upon that phosphorilation point. And then what else did we say? We also said that there was these transporters on the basolateral membrane that were pumping sodium in while you pump the calcium out into the blood to get the calcium out here into the bloodstream to increase the blood calcium levels. And it could be by the sodium calcium exchanger or it could also be due to another exchanger which is actually going to be let's put that one right here. This could be due to protons. Protons would have to come in and then this calcium ions would have to come out and this would actually depend upon the direct utilization of ATP, right? So this process right here would require ATP. Sweet deal. Okay, that was talking about the calcium reabsorption. But again, we said it was dependent upon parathyroid hormone. You know what else is really cool about the parathyroid hormone? that he's not only causing this calcium reabsorption, he also deals with phosphates in the blood. So, you know, in certain situations, where's phosphate actually reabsorbed? Come here for a second. Phosphate is actually reabsorbed right here. Let's draw phosphate in a let's do this one in we'll actually just do this one in black. So, here's phosphate, right? So, you have and usually it's in the form of HP4 2 negative, right? Monohydrogen phosphate. And what happens is this phosphate can actually naturally get reabsorbed into the bloodstream. Actually a good portion of about 85% of it is actually reabsorbed within the proximal convoluted tubule. But if the parathyroid hormone is present, if the parathyroid hormone is present, what it'll actually do is is it'll actually cause phosphate excretion. So what the parathyroid hormone will come over here and do is it will inhibit this process. If it inhibits this process, the phosphate is lost in the air. Ain't that cool? Yeah. All right, let's come back over here for a second. Another thing that I want to talk about here is right here. This what was this structure here? Remember we called this the vasa recta. We also had another special name for it. He was also called the counter current exchanger. Right? He wasn't responsible for making the medularary interstitial gradient. This whole nice saltiness of the medulla. He helped to maintain it, right? To prevent the rapid removal of the sodium chloride. How did he do that? Remember we said some of that salt, that sodium was pumped out here. That potassium was pumped out here. The two chloride ions were pumped out here. Well, what happens is as you move down again, what's that meary interal gradient? Like 300, 500, 700, 900, 1200 about, right? And this is in millos moles. As you go down, it gets saltier. So what likes to happen then? As you go down, if you think about it, if it's really, really salty, who's going to want to leave? Water. Water loves this salty stuff. So, as you're coming down, water is actually going to start leaking out into this actual medularary interstitial space. Okay? And then salt is going to be really, really rich in this area. So, it's going to actually move in. So, what will happen to this actual salt? The sodium and the chloride ions will move in. And if you think about that as you're going down, it's trying to equilibriate with the actual medularary interstitial gradient. So for example be 300 here, 500 in here, 700 in here, 900 here, and 1,200 here. But then when it makes the turnover here, something really cool happens. The exact opposite occurs. Now the water is going to want to come back in. As the water starts coming back in, a little bit of the salt is actually thrown back out. But here's what's really cool. As the salt is thrown back out into the medulla to prevent the rapid removal, he keeps a little bit of that salt. A little bit. You want to know how much? Okay. Well, what was it going in? It should be 300 millosmals. That's what we said that the plasma osmolality is leaving. It's just a little bit higher. 325 millosmles. So he helps to contribute to the rapid removal of the sodium and chloride from this medularary interstatium to help to contribute and maintain the medularary interstatial gradient. Okay, sweet deal. That was there with the countercurren exchanger. Then we got into the late distal tubule and that one we also said was actually very dependent upon a hormone. What was that hormone? That hormone was actually going to be aldoststerone, right? And we said aldoststerone was actually produced by what? It was produced by the adrenal cortex. And we said there was a special part of the adrenal cortex here, right? It was called the zona glomemeillosa. And we said the zona glomemeilosa is producing aldoststerone. And aldoststerone is usually stimulated whenever there's presence of angotensin 2 or if the sodium levels in the blood are low. Remember we said if the sodium levels in the blood are low and the potassium levels in the blood are high that could stimulate the release of aldoststerone as well as angio tensin 2 is a stimulator of this. Okay. And this is a stimulator. Okay. Aoststerone's released. What does he do? We're not going to go over the whole mechanism. We already did that. We're going to say that he just stimulates special genes, right? And those genes lead to the production of three different proteins. One of the proteins was to get what? Get the sodium in. Then we said that it developed another protein. And this other protein that it made was designed to be able to pump three sodium out and two potassium in. So he's increasing the expression of these sodium potassium pumps, right? And these pumps required ATP because they're pumping things against their concentration gradient. What else do we say? It also made these channels for the potassium to excrete the potassium out. Right? So this potassium that was really high in the blood is actually getting pumped out into the filtrate. And the sodium that was really low in the bloodstream, we're increasing it by bringing more sodium into the bloodstream. Okay? So we're trying to bring the sodium up and put the potassium down. What why is angotensin 2 being stimulated? Because we have low blood pressure. So there might not be enough water in the bloodstream. If we bring more water in, we can increase the blood volume and increase the blood pressure. How does that happen? Remember there's another structure here. Let's draw this structure and about mammalary bodies hypothalamus anterior and posterior pituitary. They're not testicles, I promise. We said that there's these specialized osmo receptors that are stimulated, right? Usually do they call the organo vasculosum of lamineris a subfrenicular organ. They stimulate the supra optic nucleus and trigger the release of antidoretic hormone. Whenever the plasma osmolality is what? Whenever you have a high plasma osmolality. What does that mean? Osmolality. Osmolality means whenever you have a high plasma osmolality that means that you have a lot of salt and very little water. So what are we going to do? We're going to release antidotetic hormone. Antidatitic hormone is going to work in the the collecting duct the deeper parts of it and the cortical part here or like the late distal tubule. So look what happens here. Antidotic hormone can come over here and it can stimulate this cell to do what? To make special aquaporins like aquaporin 2. So if we make these aquaporin 2 molecules, what is that going to do? That's going to open up these channels, right? They're going to make these channels that can pull water with it. And if the water is flowing in, what's going to happen? And the water can actually go into the bloodstream. And if the water goes into the bloodstream, what happens to the actual blood volume? Increases the blood volume, which does what to the blood pressure? Increases the blood pressure. All right? Sweet deal there, right? So again, eldoststerone does what? Three things? Increases the sodium potassium pumps. Uh makes these sodium channels to bring sodium in and makes these actual potassium channels to put potassium out. And in the presence of antiduretic hormone it can express aquaporn twos which can bring the actual water in increase blood volume and increase blood pressure. All right. In the same way antidetic hormone can act on the cells of the collecting dock. Look how he does it here. Remember we actually showed you that antidetic hormone we comes over here and binds onto V2 receptors. And remember these V2 receptors of the vasop prein receptors activated a G-proin activated adenolate cylace which did what? Turned ATP into cyclic AM and the cyclic AMP activated protein kynise A. You guys already know this. What happens? It increases the expression. I'm sorry, not the expression. It actually activates by phosphorolating these specialized proteins on these vesicles. Right? Remember, it activates these specific proteins on the vesicles. Let's show these proteins here in red. Let's say here's these proteins on the synaptic vesicles. And what does protein kinus A do? Protein kynis A comes over here and actually phosphorolates them and stimulates them to migrate to the membrane. And what happens? It plugs into the membrane these little aquaporins. And again, this is aquaporin 2. And then what starts coming in? Water. And if water starts flowing in, what's going to happen? The water will flow into the actual tubial cells. And then there's these aquaporn 3 and four proteins we said on the basilateral membrane. What will happen? The water will go into the bloodstream. As the water goes into the bloodstream, what happens to the actual blood volume? You get an increase in blood volume which increases your blood pressure. What else did we say? Well, originally the plasma osmolality was high. It was very hypertonic. If we bring more water in, we bring the plasma osmolality down back to a normal range of approximately 300 millosmals. Okay. What else did we say? Remember we had the intercolated A cells and intercolated B cells and they were functioning during metabolic acidosis and alkalossis. Remember what they were doing? Remember we had the A cell let's say this is the intercolated A cell. Remember it was actually taking the CO2 combining with water to form carbonic acid, right? And then if you remember carbonic acid which was H2 CO3 which can disassociate into protons and bicarbonate and we said remember intercolated A cells is for acidosis. So what does that mean? We can pump protons out and who do we bring in? A little bit of potassium. Right? Then what do we say? If this acidosis, that means that the blood pH is really low. Well, what are we going to do? We're going to bring by cararb into the blood. And what are we going to do to prevent excessive changes in the ions moving across this membrane? We're going to bring chloride ions in. If we bring a lot of bicarb, what's it going to do to the pH? It's going to bring the pH back up to normal ranges. Okay, that was one of the things we said. Then what else? Remember, we had the intercolated B cell. This was the B cell and it was for basic conditions or metabolic alkyossis, right? Same concept. What do we say here? CO2 combines with water. When that happens, what do you get? You get carbonic acid. This is driven by the carbonic anyhydrates enzyme. And again, this is driven by the carbonic anyhydrates enzyme. This breaks down into bicarbonate and into protons. What do we say is the difference here? Now we excrete out the bicarb and we bring in the chloride ions, right? To prevent the excessive change there. Then what do we do? We push the protons out here. Why? Because we said that the blood is in a basic situation. What does that mean? That means that the pH is high. If we bring a lot of these protons in, what is it going to do? It's going to bring the pH back down. Okay? And that's how our body deals with this metabolic acidosis and alkalossis situations. What else did we say? Remember we also said that there can also be a little bit of uh certain substances that can be secreted out in this area too. If I draw one more cell here, remember we said that we can actually have excretion of drugs. We can actually excrete out ammonia. Remember we have ammonia and it can combine with one of these protons out here. Like for example, this proton here. Let's say it combines with this proton that actually got pushed down. What can we get out of this? If these two react, we get ammonium. And what else did we say that we could excrete too? It could also excrete creatinine. All right. And there's even other substances that could also be excreted like uric acid and even a little bit of other uh nitrogenous waste products. One more thing at the end part of the collecting duct, what was that molecule that actually was left over? A lot of water was lost. So, as a lot of water was lost, that's to extend this actual collecting duct down a little farther here. And we get down as we get down to the bottom part, there's just a little bit of a this substance left over. What color do we make him? Let's make him green. This substance is called ura. Remember URA was absorbed within the actual what the proximal convoluted tubule. Well, some of the ura is actually reabsorbed here at the end of the collecting duct. And what do we say the ura is doing? We said some of that ura is actually being recycled. Remember, it's actually moving over here. And as it's moving over here to get recycled, what happens? Some of that ura might accumulate here in the meillary interstitial space. And ura is a solute. It's more of a lipid soluble solute, but still nonetheless it can attract water because it can contribute to the medularary interstatial gradient. What is that going to do? That's going to allow for more water to flow out of what? More water to flow out of the descending limb. So, it's going to contribute to making concentrated urine. So, again, what is this process here called? It's called ura recycling. All right, sweet deal. And again, a lot of that ura could actually get lost in the urine as well, as well as other substances that we'll talk about during the mcturation reflex when we talk about the composition of the urine. Okay, so in a nutshell, guys, we covered a lot of this stuff here, right? One thing I didn't finish off with is this sodium and water. I'm sorry. 20% of the water right is remaining 20% of the water because 65% of it was reabsorbed here in the PCT and about 15% of it was reabsorbed here in the loop of Henley specifically the descending the remaining water that's left over is dependent upon the presence of antidotic hormones so the amount of water that you reabsorb is variable the sodium there's about 10% of the actual sodium remaining this sodium a small percentage about 5 to 6% of the sodium is actually through the sodium chloride simporter. The remaining uh four to 5% is dependent upon the actual aldostrone. Okay. And then we said that calcium was dependent upon the parathyroid hormone. All right. In this video, we covered a lot of information. We covered basically everything that we covered throughout the series of videos. I hope all of it made sense. I really hope you guys enjoyed it. If you did, please hit the like button, comment down the comment section, and subscribe.