Renal Physiology: Regulation of Glomerular Filtration
25. The Urinary System
Renal Physiology: Regulation of Glomerular Filtration - Video Tutorials & Practice Problems
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Introduction to Regulation of Glomerular Filtration
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OK. So I've been talking for a while about how important it is to maintain glomerular filtration rate and keep it pretty consistent. And now we're finally gonna get into how our body actually does that. So here we're just gonna do a quick introduction into this idea of regulation of glomerular filtration. And then we'll have some more specific examples coming up for you as well. The glomerular filtration rate is regulated by a number of mechanisms and they can be divided into two main categories. So first, we have our internal factors, internal meaning internal to the kidney. And these are also called renal autoregulation or even just auto regulation. And so what's happening here is that the kidneys regulate renal blood flow all on their own. So they are monitoring glomerular filtration rate um and making sure that it stays consistent. And so these are gonna be maintaining glomerular filtration rate directly and our kidneys are gonna be able to all by themselves, keep glomerular filtration rate pretty consistent through any normal changes in blood pressure and by normal changes in blood pressure, I mean, things like if I was sitting down for a long time and then I stood up kind of quickly or if I went for a nice casual walk around the block, you know, just daily changes in blood pressure in healthy individuals. And there are two main examples of this that we're gonna have videos for. We have our myogenic mechanism and our trullo glomerular mechanism. Now, I'm kind of shifting gears over to our external factors. These are gonna be factors that are designed to maintain systemic blood pressure. And so they're gonna be maintaining glomerular filtration rate. Indirectly, we've talked a lot about how glomerular filtration rate and systemic blood pressure are correlated. And so by maintaining that systemic pressure, these factors will be indirectly affecting our glomerular alteration rates. And these are gonna be adjusting glomerular filtration rate following much more significant changes in blood pressure, blood volume or electrolyte imbalances. Now, quite often textbooks use the example of like if a person is hemorrhaging or has a really severe injury and these factors are gonna kind of kick in. Um but I do want to be clear, it can happen in less extreme situations as well. So if you're doing like a very intensive workout or if you've been, you know, kind of sick for a few days and you haven't really ate or drank very much and you are kind of dehydrated and low in electrolyte, then that you know, those situations could also make these external factors kind of kick in and affect glomerular filtration as well. So it does not have to be like a life threatening situation. And there are two main external factors that we're gonna talk about here. We have neural mechanisms as well as the renin angiotensin aldosterone mechanism. And all four of these mechanisms are going to work by controlling the diameter of either the afferent or efferent arterial. So basically affecting how much blood is getting into the glomerular capillaries or exiting those capillaries. And we're gonna be talking about that in our next video. So I'll see you there.
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example
Renal Physiology: Regulation of Glomerular Filtration Example 1
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All righty. So this one asks us, generally speaking, renal autoregulation maintains glomerular filtration rate blank. Whereas external factors regulate glomerular filtration rate blank. Let's run through the answers and see what we have. So A is directly or renal autoregulation and then indirectly or external factors and looks like we got it in one. That is the correct answer. So remember, renal autoregulation is going to be our kidneys monitoring glomerular filtration rate and making any changes as needed to directly affect it. Whereas external factors are factors that impact systemic blood pressure. And then because of that, they naturally affect glomerular filtration rate. Indirectly. The right answer is a, that is the reason B would be incorrect. Um C we obviously do not have any conscious control over our glomerular filtration rate. OC is out and then D slowly and quickly, we need all of these to work pretty quickly. And if anything, the renal autoregulation will be a little bit quicker since that's directly impacting um the glomerular filtration rate. So D would be out as well. And that is why our answer is a
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Arteriolar Diameter and GFR
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In this video, we're gonna be talking about how changes in arterial or diameter can affect glomerular filtration rate. Now, what is actually happening is that changes in arterial or diameter of either the um affluent or efferent arterials actually directly affect glomerular filtration pressure, which then in turn directly affects amear filtration rate is remember those variables are positively correlated. So if one goes up, the other goes up, if one goes down, the other goes down. Now, as I've mentioned a few times, I know that the anatomy in this chapter can be a little confusing looking. I know that there's a lot of moving parts to keep track of. And when I was first learning this, it really helped me to kind of just take a step back and use a metaphor to help me picture what was going on in my head um because it can be confusing. So I want to share that metaphor with you here and hopefully it can be helpful to you. So bear with me for a moment. But I want you to imagine that the glomerular capsule is a stink and in our sink metaphor, the faucet is going to be the affluent arterial, right? So the faucet is where water would arrive. The affluent arterial is where blood would arrive. The basin of the sink is going to be the glomerulus. Though our big old voc capillaries and then the drain where water would exit is going to be our um efferent arterial where blood will be exiting from. So we're gonna go through what vasodilation and vasoconstriction of the afferent and arterials would look like. And with, within this metaphor and how they would be affecting glomerular filtration pressure and glomerular filtration rate. So, if we were to have vasoconstriction of our affluent arterial, I want you to imagine that we have basically turned the faucet down. So as you can see, now, very little water is coming out of that faucet and um not much water is going to accumulate in that basin. And that's what's happening in our glomerulus because of the constriction of that ent arterial blood just can't really get into the glomerulus in the first place. And so, not very much is accumulating in there. And because there's just less blood, we're going to have a decrease in filtration pressure which will lead to a decrease in f infiltration rate. Now, if we were to have basal dilation of our arterial, I want you to imagine that we are now turning the faucet up. So now water is pouring into the sink and it's pouring into the sink faster than it can drain And so the basin is beginning to fill up a little bit and that's what's happening within our glomerulus though, if our affluent arterial is dilated, a ton of blood is rushing into that glomerulus faster than it can actually drain out. And so we're gonna have an increase in pressure and an increase in filtration rate as a result of that. Now switching gears to our efferent arterial. If we were to have vasoconstriction of our efferent arterial, I want you to imagine that our drain is now logged if, though our drain is clogged and if we were to run the faucet at all, the water will just be accumulating in the basin because there's nowhere for it to go to, to be draining out of that. And that's what's gonna happen in our anatomy. So, if we were to have in friction of that efferent arterial blood just can't get out of the glomerulus. And so we're gonna have a backup where blood is still coming in, but it can't get out. And so that's gonna lead to an increase in pressure as well as an increase in filtration rate. Now, if we were to have vasodilation of our efferent arterial, I want you to imagine now that somebody built this sink, but they did not do a very good job and the drain of the sink is just way too big. And so no matter how high you put that water on water can never accumulate in the basin because it's, it's gonna just go straight out of that drain. That's kind of what's happening here. Our efferent arterial is now so dilated that blood is just rushing out of the glomerulus. And so because blood is rushing out and not really accumulating in there, we're gonna have a decrease in glomerular filtration pressure and a decrease in glomerular filtration rate. So hopefully, this is helpful to you. We did include some images of spins on some upcoming videos as we go over more specific regulation mechanisms to help you kind of track the metaphor as we go along and I will see you guys in the next one. Bye bye.
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concept
Internal Regulation - The Myogenic Mechanism
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All right. So we're gonna get started on that myogenic mechanism. So this is an internal regulation technique. So this is the kidneys engaging in autoregulation and maintaining that glomerular filtration rate all on their own. Though the myogenic mechanism adjust the affluent arterial in response to normal minor daily changes in blood pressure. So, if you recall from a few chapters back to help us maintain homeostasis, vascular smooth muscle responds to changes in blood pressure. And so it's going to contract when it's stretched and it relaxes when it's not stretched. And that is actually where the name of this mechanism comes from. Remember that myo means muscle. And so the myogenic mechanism reflects a property of vascular smooth muscle in our body. Though our main stimulus here is going to be stretching or a decrease or absence of stretch within our afferent arterial. And that is going to basically signal to the kidneys whether blood pressure has increased or decreased. So I'm gonna walk you through exactly what would happen um if there was an increase or a decrease in blood pressure. So first we imagine that we have an increase in systemic blood pressure. This increase in blood pressure would lead to an increased stretch in the smooth muscle of the afferent arterial because more blood is coming in blood is coming in faster. And that is, it's gonna stretch that vascular smooth muscle. Now, that would trigger this reflex and the arterial would contract the contraction or the um of the affluent arterial is going to restrict blood flow into the glomeruli. And by doing that, our glomerular filtration rate will be maintained at a normal range. Though, if we go down to our little image here again, just picture, we are constricting that arterial, which is the equivalent of turning down the sink and now less blood can get into the glomerulus. So even though blood pressure in the whole body has increased, the glomerulus is receiving the correct amount of blood to maintain a glomerular filtration rate. So, if we look up here, if we were to have a decrease in systemic blood pressure, we would have decreased stretch in the smooth muscle of the aurate arterial. And so our arterial would relax and that relaxation or dilation would increase blood flow into the glomerulus. And our GFR would be maintained at a normal range. So once again, imagine we are dilating that parent arterial, we're like turning up the faucet basically. And so even though the stomach blood pressure has decreased, the kidneys are receiving the correct amount of blood to maintain glomerular filtration rate. All right. So that is our myotonic mechanism and I'll see you guys in the next one. Bye bye.
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example
Renal Physiology: Regulation of Glomerular Filtration Example 2
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OK. So this is a true or false. If it's false, we're gonna be finding the answer that would correct the statement. So the main stimulus that triggers the myronic mechanism is a high concentration of sodium delivery to the glomerular capillaries and that is false. That is incorrect. This mechanism does not respond to sodium levels at all. So, right away, um A and D are both out keep in mind that my o literally means muscle. And so this mechanism is reflecting a property of certain vascular smooth muscle which um has the reflex where it will contract if it, if it detects stretch and it will relax if it detects a lack of stretch or a decrease in stretch. So based on that looks like B and C are pretty neck and neck. But remember, the purpose of this mechanism is to detect changes in systemic blood pressure. So the blood coming into the kidney will tell us that information. And so it must be our afferent arterial because that is where the blood is arriving, right. So based on that, our answer is going to be c the main stimulus that triggers this mechanism will be an increase or decrease of stretch in the afferent arterial.
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Problem
Problem
The myogenic mechanism is triggered by changes in the stretch of the afferent arteriole. This is the direct result of:
A
Changes in glomerular filtration rate.
B
Changes in glomerular pressure.
C
Changes in systemic blood pressure.
D
Electrolyte levels.
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concept
Internal Regulation - The Tubuloglomerular Mechanism
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OK, let's get into that tub beo glomerular mechanism and this is still renal autoregulation. So this is our kidneys still handling things on their own. And I know that tullo glomerular is quite a mouthful, but it's actually a very intuitive name. So broadly, what's happening here is that our renal tubule is acting on the glomerulus in order to change blood flow. So not the most fun word to say but in an intuitive naming convention at least. So this is basically gonna be a secondary mechanism that will adjust the affluent arterial in response to minor changes in blood pressure. And I say secondary mechanism because basically, if our myogenic mechanism is not quite enough to get glomerular filtration rate back to where it needs to be, this will kick in to kind of help with that process. And so as you may recall from when we were first learning about nephrons, macula denso cells in the renal tubule respond to sodium chloride level. You guys remember these um macula denso cells, you can see them here in green. Those are those very tightly packed cells that are right at the transition point of the ascending limb and distal tubule. And as a result of that, they're located very close to the afferent and efferent arterial um in location. So our main stimulus here is going to be changes in the levels of sodium chloride near those macula denso cells. So just like with our last video, I'm gonna walk you through what would happen um If we had an increase in blood pressure as well as a decrease in blood pressure. So, if we were to have an increase in systemic blood pressure, what's gonna happen is that as GFR increases filtrate volume also increases. Now, we just have more filtrate flowing through our renal tubule. And that is going to cause an increased delivery of sodium chloride to our maculate denso cell, more filtrate just means more sodium chloride in that filtrate. And so that is gonna be our main stimulus. And then as a result of that, our macula denso cells are going to release vasoconstrictor chemical, those are going to lead to the constriction of the affluent arterial. And then that is going to mean that over time, our GFR will be decreased back down to a normal range because less blood flow can get into that glomeruli. Now, if we were to have a decrease in systemic blood pressure, what's gonna happen is the opposite. So as GFR decreases, filtrate volume also decreases, which means we have decreased delivery of sodium chloride to our macula denser cell. So just less filtrate means less sodium chloride at getting to those macula denser. And so what's gonna happen here? That is gonna be our stimulus. And then the macula denser cells will basically stop releasing any kind of vasoconstrictor chemical. And then as a result of that, we're going to have some dilation or relaxation of our afferent arterial and then that dilation is going to lead to our GFR getting increased back up to a normal range as blood flow increases into the glomeruli. All right. So that is our tubular glomerular mechanism and I will see you guys in our next video. Bye bye.
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example
Renal Physiology: Regulation of Glomerular Filtration Example 3
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OK. So for this one, we're gonna be filling in the blank. So increased delivery of sodium chloride to the macula denis cells is indicative of blank. This would trigger the tubular glomerular mechanism which would cause blank of the aberrant arterial kind of work through that for a second. So if we have increased delivery of sodium chloride to our macular denso cells, that would be indicative of an increased glomerular filtration rate. If we have an increased filtration rate, we're gonna have an increase in filtrate volume, which just means more sodium chloride around those macula denso cells. So based on that, we're working with either B or D and then that would trigger this mechanism which would release vasoconstrictor chemicals to try and constrict that affluent arterial. So it looks like our answer is going to be be here. Remember we would want to constrict that arterial because that would basically um allow for less blood flow to come into our glomerulus, which would decrease filtration pressure, which would decrease filtration rate and get everything back to normal. Though our answer here is going to be B
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concept
External Regulation – Neural Mechanisms
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Now, we're gonna start talking about external regulation and we're gonna begin with neural mechanisms though our stimulus here is going to be increased empathetic nervous system activity and it's basically going to override renal autoregulation. So when we are in some kind of fight or flight situation, the sympathetic nervous system will basically totally take over the body in that moment. And so sympathetic activation is going to trigger the release of norepinephrine and norepinephrine is going to constrict any blood vessels in non-essential organs. And that includes our afferent and efferent arterial. So when both the E and efferent arterials are constricted, we end up with a decrease in glomerular filtration rate. If you look at our image here, if we have constriction in our affluent arterial, imagine basically that we have turned the sink down right low is restricted though not very much blood is getting into that glomerulus. And if we have constriction of our efferent arterial kind of like our drain is logged though not much blood can get in but not much blood can get out either. Basically, this entire process is just sort of stunted at the moment and can't really do very much. And the purpose of this is to help the body minimize fluid loss. We don't wanna be prioritizing, making urine if we're in some kind of emergency situation, right? This is why we typically don't need to urinate during a fight or flight um situation. This will also help to preserve blood volume and blood pressure at more vital organs. So it has a very important evolutionary function. All right. So that is our first external regulation mechanism and I'll see you guys in our next video. Bye bye.
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example
Renal Physiology: Regulation of Glomerular Filtration Example 4
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OK. So activation of the sympathetic nervous system leads to a decrease in glomerular filtration rate. Why is decreasing GFR advantageous and potentially stressful, dangerous or arousing situation? Let's run through our answers and see what we have here. So a reads that by reducing glomerular filtration rate, the body prevents hypertension. That's actually not true at all. That's actually the opposite of how it works. Though, if we decrease glomerular filtration rate, we are retaining fluid and over time if there's like a chronic um decrease in filtration rate, that fluid retention can actually cause hypertension not prevent it. So A is definitely out and not as incorrect. Also, B is by increasing fluid loss, it makes you lighter in case you have to run away from danger. Tempting, given that whole fight or flight idea. However, um decreasing glomerular filtration rate would not increase fluid loss. We're basically putting urine production like on hold right now, we are not increasing it. So B is also out, he reads, it helps minimize fluid loss and preserves blood volume and blood pressure at vital organs and that is absolutely correct. So, if you were in a fight or flight situation one making urine is just not a priority. And this allows you to retain any fluids that could be essential if you were to like get dehydrated, for example, and it helps you preserve blood volume and pressure at important organs like your brain and your heart. Or our answer is probably c let's just check DD reads. It actually is not advantageous but is a leftover quirk of evolution. And that is not true or the reason I just explained. So our answer here is going to be B.
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Problem
Problem
The sympathetic nervous system releases _____________, which causes constriction of the afferent and efferent arterioles.
In this video, we're gonna be going over the Renan Anteo tens and Aldosterone system also known as the Rasp. And I'll be honest, this one can be a little bit of a doozy. There is a lot of steps in this mechanism. It has multiple effects on the body and there is some kind of big terminology to keep track of. So I would encourage you to take your time with this video, pause it if you need to and you and I will get through this together. So no worries. So as you may have heard previously in your A MP course, the ren and angiotensin aldosterone system is the body's main mechanism for increasing blood pressure. So our main stimulus here is going to either be sympathetic activity or the detection of low blood pressure. And I know that at first glance, those can kind of seem like opposites, we think like fight or flight, increase blood pressure. But keep in mind from the perspective of a kidney which would receive less blood flow during sympathetic activity. These are basically the exact same thing. So we're gonna go through how the mechanism works. And one nice thing to keep in mind is that it basically is named in the order that substances will appear. So first we're gonna see Renan, then angiotensin and then aldosterone. So keep that in mind as we go through the. So first up our blood pressure is going to decrease, we're gonna have less blood flow to our kidneys, whatever happens. And then as a result of that, our macular dens of cells will detect low glomerular filtration rate because they're gonna be receiving less um sodium chloride. The macula denis cells will then signal to our kidneys. Hey, we have to release the enzyme Renan into the bloodstream. So the kidneys release Renan and there is the first piece of our name. So then renin is going to go to the liver where it convert angiotensinogen into angiotensin. One, angiotensin. One will then travel to our lungs where it gets converted into angiotensin two and angiotensin two is gonna be really the main player here. So there is the angiotensin piece of our name and angiotensin two has widespread effects on the body in order to increase blood pressure. So it's gonna be directly increasing blood pressure. It's gonna be increasing blood volume as well as having a direct effect on glomerular filtration pressure and rate. So it's gonna be very busy. Now, we're gonna start over here talking about how it directly impacts systemic blood pressure. And it does that through the vasoconstriction of systemic blood vessels. You can imagine we're gonna have constriction here. So it's kind of like taking a garden hose that's already on. You took that hose and kind of squeezed it and kind of constricted it. You can imagine how the water coming out of it is gonna be coming at a much higher pressure and that's what's happening in your body there. Right off the bat. We have this increase in blood pressure as a result of that vaso constriction. Now moving over to this middle piece, we're also gonna be increasing blood volume, which remember increasing blood volume is going to indirectly impact our blood pressure by increasing it as well. So we have this dotted line here to kind of symbolize how increasing blood volume will also help increase blood pressure. And um angiotensin two increases blood volume in two ways. So we're gonna start over here and that angiotensin two is going to be promoting the reabsorption of sodium in the proximal tubule of our Nephron. Remember, reabsorption is when we take a substance out of the filtrate and put it back into our bloodstream. So by promoting a reabsorption of sodium that is also going to cause the reabsorption of water by osmosis, we'll talk about this in some unsung upcoming videos. But long story short, basically, water wants to follow high folly concentration. So if water sees a whole bunch of sodium leaving the filtrate and going back into the blood water wants to follow it. So we're gonna have a whole bunch of water entering our blood, which of course, will increase our blood volume. So that's what's happening in the proximal tubule. Now, angiotensin two, we're gonna move over here. Now, angiotensin two is also gonna promote the release of aldosterone, the last piece of our name there and aldosterone increases the reabsorption of sodium as well. But it is going to do so in the distal tubule and the collecting duct. And so we're also working kind of in this opposite end of the Nephron. And that's gonna have the exact same effect. It's gonna cause water reabsorption by osmosis there as well. So now we have in basically the majority of our Nephron, we have increased water reabsorption. We have a whole bunch of water entering our blood, which will of course impact our blood volume. You can imagine our garden hose, we have our hose, it's on, we're already squeezing it and kind of constricting it. Now someone comes and turns up the faucet even higher. So we have an even higher volume of water coming through this little constricted hose. You can imagine the way that that would impact the pressure coming out of it. And that is basically what's happening in your body right now. So that is kind of the systemic widespread effects that angiotensin two is gonna have. Now, one quick note before we move on is that I know that, um, you know, this piece of it can kind of feel like splitting hairs where you're like. All right. So the angiotensin two does sodium reabsorption in the proximal tubule, but the aldosterone is doing it over here kind of hard to keep of. One thing that, that has always helped me is to think like aldosterone that hard, like the sound. And I think like aldosterone distal tubule, collecting duct, I think of all those d words kind of coming together and that has always helped me, hopefully it can help you as well. All right. So moving over to the last piece over here, we're gonna talk about how angiotensin two can directly impact glomerular filtration pressure and rate. And it does that through the vaso constriction of the efferent arterial. So we've been talking a lot about our affluent arterial, but now we are over here in the efferent arterial. And so remember this is kind of like clogging the drain. So what's happening is that we're gonna have this kind of backup or build up of blood in that glomerulus, which will then increase glomerular filtration pressure and the um glomerular filtration rate. And so our angiotensin two is really having various widespread effects throughout the body uh as well as directly in the kidneys, all of which are working toward increasing and raising that systemic blood pressure. All right. So you did it fantastic job. We got through the Ren and angiotensin aldosterone system and I will see you guys in our next video bye bye.
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example
Renal Physiology: Regulation of Glomerular Filtration Example 5
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OK. So which of the following hormones is responsible for increasing reabsorption of sodium in the distal tubule and the collecting duct. All right, let's run through our answers here. So first, we have angiotensin one. Angiotensin one is not gonna have any major effects. That's just gonna need to get converted to angiotensin two. So that is definitely out. Now, remember angiotensin two is going to increase sodium reabsorption in our proximal tubule, but it's not going to directly affect any sodium reabsorption anywhere else in our renal tubule or collecting duct. Though angiotensin two is out B is aldosterone and that one is correct. Remember though the D sounds aldosterone distal tubule collecting duct, they all kind of go together. Our answer here is the aldosterone parathyroid hormone does operate in the distal tubule, but it is focusing on calcium, not sodium. So our answer here is going to be c aldosterone.
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Problem
Problem
Angiotensin-II directly increases glomerular filtration pressure by _____________ the ___________ arteriole.
A
Constricting; afferent.
B
Constricting; efferent.
C
Dilating; afferent.
D
Dilating; efferent.
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