Renal Physiology: Regulation of Glomerular Filtration - Online Tutor, Practice Problems & Exam Prep

Glomerular filtration rate (GFR) is regulated by internal mechanisms like the myogenic and tubuloglomerular responses, which adjust arteriolar diameter to maintain consistent blood flow. External factors, including the neural mechanism and the renin-angiotensin-aldosterone system (RAAS), respond to significant blood pressure changes. RAAS increases blood pressure through vasoconstriction and sodium reabsorption, enhancing blood volume. Understanding these mechanisms is crucial for grasping renal function and homeostasis.

Introduction to Regulation of Glomerular Filtration

Okay. 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 going to get into how our body actually does that. So here we're just going to do a quick introduction into this idea of regulation of glomerular filtration. Then we'll have some more specific examples coming up for you as well. So glomerular filtration rate is regulated by a number of mechanisms and they can be divided into 2 main categories. So first, we have our internal factors, internal meaning internal to the kidney. These are also called renal autoregulation or even just autoregulation. 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, and making sure that it stays consistent. And so these are going to be maintaining glomerular filtration rate directly. And, our kidneys are going to 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 a healthy individual. There are two main examples of this that we're going to have videos for. We have our myogenic mechanism and our tubuloglomerular mechanism. Now, kinda shifting gears over to our external factors. These are going to be factors that are designed to maintain systemic blood pressure. And so they're going to be maintaining glomerular filtration rate indirectly. So 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 filtration rate. And these are going to be adjusting glomerular filtration rate following much more significant changes in blood pressure, blood volume, or electrolyte imbalances. Now, quite often textbooks, you see an example of, like, if a person is hemorrhaging or has a really severe injury, then these factors are going to kind of kick in. 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 eaten or drank very much and you are kind of dehydrated and low in electrolytes, 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 2 main external factors that we're going to talk about here. We have the neural mechanism as well as the renin-angiotensin-aldosterone mechanism. And all 4 of these mechanisms are going to work by controlling the diameter of either the afferent or efferent arteriole. So basically affecting how much blood is getting into the glomerular capillaries or exiting those capillaries. And we're going to be talking about that in our next video. So I'll see you there.

Renal Physiology: Regulation of Glomerular Filtration Example 1

Alrighty. So this one asks us, generally speaking, renal autoregulation maintains glomerular filtration rate directly, whereas external factors regulate glomerular filtration rate indirectly. Let's run through the answers and see what we have. So a is directly for renal autoregulation and then indirectly for external factors and it looks like we got it in one. That is the correct answer.

So remember, renal autoregulation is 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. So our answer is a. That is the reason b would be incorrect. C, we obviously do not have any conscious control over our glomerular filtration rate.

So c 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 the glomerular filtration rate. So d would be out as well, and that is why our answer is a.

Arteriolar Diameter and GFR

In this video, we're going to be talking about how changes in arteriolar diameter can affect glomerular filtration rate. Now, what is actually happening is that changes in arteriolar diameter of either the afferent or efferent arteriole directly affect the glomerular filtration pressure, which then in turn directly affects the glomerular filtration rate. As 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 understand what was going on in my head 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 sink. And in our sink metaphor, the faucet is going to be the afferent arteriole. Right? So the faucet is where the water would arrive; the afferent arteriole is where blood would arrive. The basin of the sink is going to be the glomerulus, so our big old ball of capillaries. And then the drain, where water would exit, is going to be our efferent arteriole, where blood will be exiting from.

We're going to go through what vasodilation and vasoconstriction of the afferent and efferent arterioles would look like within this metaphor and how they would be affecting the glomerular filtration pressure and glomerular filtration rate. So, if we were to have vasoconstriction of our afferent arteriole, 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 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 afferent arteriole, 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 filtration rate.

Now, if we were to have vasodilation of our afferent arteriole, 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, so the basin is beginning to fill up a little bit and that's what's happening within our glomerulus. So if our afferent arteriole is dilated, a ton of blood is rushing into that glomerulus faster than it can actually drain out. And so we're going to have an increase in pressure and an increase in filtration rate as a result of that.

Now, switching gears to our efferent arteriole. If we were to have vasoconstriction of our efferent arteriole, I want you to imagine that our drain is now clogged. So our drain is clogged, and if we were to run the faucet at all, the water would just be accumulating in the basin because there's nowhere for it to go to be draining out of. And that's what's going to happen in our anatomy. So if we were to have constriction of that efferent arteriole, blood just can't get out of the glomerulus. And so we're going to have a backup where blood is still coming in, but it can't get out. And so that's going to lead to an increase in pressure as well as an increase in filtration rate.

Now, if we were to have vasodilation of our efferent arteriole, 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 going to just go straight out of that drain. That's kind of what's happening here. Our efferent arteriole is now so dilated that blood is just rushing out of the glomerulus. And so because the blood is rushing out and not really accumulating in there, we're going to have a decrease in glomerular filtration pressure and a decrease in glomerular filtration rate.

Hopefully, this is helpful to you. We did include some images of sinks in some upcoming videos as we go over more specific regulation mechanisms to help you track the metaphor as we go along, and I will see you guys in the next one. Bye bye.

Internal Regulation - The Myogenic Mechanism

Alright. So we're going to get started on that myogenic mechanism. This is an internal regulation technique. It involves the kidneys engaging in autoregulation and maintaining the glomerular filtration rate all on their own. The myogenic mechanism adjusts the afferent arteriole in response to normal minor daily changes in blood pressure. If you recall from a few chapters back, to help us maintain homeostasis, vascular smooth muscle responds to changes in blood pressure; it contracts when it's stretched and 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. Our main stimulus here is going to be stretching or a decrease or absence of stretch within our afferent arteriole. This is going to signal to the kidneys whether blood pressure has increased or decreased. I'm going to walk you through exactly what would happen if there was an increase or decrease in blood pressure.

First, we're going to 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 arteriole. Because more blood is coming in faster, it's going to stretch that vascular smooth muscle. This would trigger a reflex, and the arteriole would contract. The contraction of the afferent arteriole restricts blood flow into the glomerulus. By doing that, our glomerular filtration rate will be maintained at a normal range. Now, if we go down to our little image here, again, just picture we are constricting that afferent arteriole, 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.

If we were to have a decrease in systemic blood pressure, we would have decreased stretch in the smooth muscle of the afferent arteriole. And so, our arteriole would relax. This 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 afferent arteriole, like turning up the faucet basically. Even though systemic blood pressure has decreased, the kidneys are receiving the correct amount of blood to maintain the glomerular filtration rate.

Alright. That is our myogenic mechanism, and I'll see you guys in the next one. Bye-bye.

Renal Physiology: Regulation of Glomerular Filtration Example 2

Okay. So this is a true or false question. If it's false, we're going to be finding the answer that would correct the statement. The main stimulus that triggers the myogenic mechanism is a high concentration of sodium delivery to the glomerular capillaries, and that is false. This mechanism does not respond to sodium levels at all. So right away, A and D are both out. Keep in mind that "myo" literally means muscle. And so this mechanism is reflecting a property of certain vascular smooth muscle, which has the reflex where it will contract if it detects stretch, and it will relax if it detects a lack of stretch or a decrease in stretch. So based on that, it 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 arteriole 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 arteriole.

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.

Internal Regulation - The Tubuloglomerular Mechanism

Okay. Let's get into that tubuloglomerular feedback mechanism. This is still renal autoregulation, so this is our kidneys still handling things on their own. And I know that "tubuloglomerular" is quite a mouthful, but it's actually a very intuitive name. Broadly speaking, 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 at least it follows an intuitive naming convention. This is basically going to be a secondary mechanism that will adjust the afferent arteriole 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 the glomerular filtration rate back to where it needs to be, this will kick in to kind of help with that process.

As you may recall from when we were first learning about nephrons, macula densa cells in the renal tubule respond to the sodium chloride level. You guys remember these macula densa 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. As a result of that, they're located very close to the afferent and efferent arterioles, in location. So, our main stimulus here is going to be changes in the levels of sodium chloride near those macula densa cells. Just like with our last video, I'm going to walk you through what would happen if we had an increase as well as a decrease in blood pressure.

If we were to have an increase in systemic blood pressure, what's going to happen is that as GFR increases, the 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 macula densa cells. More filtrate just means more sodium chloride in that filtrate. And that is going to be our main stimulus. As a result of that, our macula densa cells are going to release vasoconstrictor chemicals. Those are going to lead to the constriction of the afferent arteriole and, over time, our GFR will be decreased back down to a normal range because less blood flow can get into that glomerulus.

Now, if we were to have a decrease in systemic blood pressure, what's going to happen is the opposite. So as GFR decreases, the filtrate volume also decreases. This means we have decreased delivery of sodium chloride to our macula densa cells. So, just less filtrate means less sodium chloride getting to those macula densa. That is going to be our stimulus. The macula densa cells will basically stop releasing any kind of vasoconstrictor chemical. As a result, we're going to have some dilation or relaxation of our afferent arteriole, and that dilation is going to lead to our GFR getting increased back up to a normal range as blood flow increases into the glomerulus.

Alright. That is our tubuloglomerular mechanism, and I will see you guys in our next video. Bye bye.

Renal Physiology: Regulation of Glomerular Filtration Example 3

Okay. So for this one, we're going to be filling in the blanks. So increased delivery of sodium chloride to the macula densa cells is indicative of an increased glomerular filtration rate. This would trigger the tubuloglomerular feedback mechanism which would cause constriction of the afferent arteriole. We'll kinda work through that for a second. So if we have increased delivery of sodium chloride to our macula densa cells, that would be indicative of an increased glomerular filtration rate. If we have an increased filtration rate, we're going to have an increase in filtrate volume, which just means more sodium chloride around those macula densa cells. So based on that, we're working with either option B or D. And then that would trigger this mechanism which would release vasoconstrictor chemicals to try and constrict that afferent arteriole. So it looks like our answer is going to be B here. Remember, we would want to constrict the arteriole because that would basically 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. So our answer here is going to be B.

External Regulation – Neural Mechanisms

Now, we're going to start talking about external regulation and we're going to begin with the neural mechanism. Though our stimulus here is going to be increased sympathetic 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 arteriole. So when both the afferent and efferent arterioles 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 afferent arteriole, imagine basically that we have turned the sink down. Right? Flow is restricted, though not very much blood is getting into that glomerulus. And if we have constriction of our efferent arteriole, kind of like our drain is clogged. So 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 want to 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, situation. And this will also help to preserve blood volume and blood pressure at more vital organs. So, it has a very important evolutionary function.

Alright. So that is our first external regulation mechanism, and I'll see you guys in our next video. Bye bye.

Renal Physiology: Regulation of Glomerular Filtration Example 4

Okay. So activation of the sympathetic nervous system leads to a decrease in glomerular filtration rate. Why is decreasing GFR advantageous in potentially stressful, dangerous, or arousing situations? 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. It's actually the opposite of how it works. So if we decrease glomerular filtration rate, we are retaining fluid. And over time, if there's a chronic decrease in filtration rate, that fluid retention can actually cause hypertension, not prevent it. So A is definitely out and that is 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, decreasing glomerular filtration rate would not increase fluid loss. We're basically putting urine production on hold right now. We are not increasing it. So B is also out.

C reads, it helps minimize fluid loss and preserve the blood volume and blood pressure at vital organs, and that is absolutely correct. So if you were in a fight or flight situation, making urine is just not a priority, and this allows you to retain any fluids that could be essential if you were to become dehydrated, for example. It helps you preserve blood volume and pressure at important organs like your brain and your heart. Our answer is probably C.

Let's just check D. D reads, It actually is not advantageous but is a leftover quirk of evolution, and that is not true for the reason I just explained. So our answer here is going to be C.

The sympathetic nervous system releases _____________, which causes constriction of the afferent and efferent arterioles.

• A. Acetylcholine.
• B. Epinephrine.
• C. Norepinephrine.
• D. Dopamine.

External Regulation – Renin-Angiotensin-Aldosterone Mechanism

In this video, we're going to be going over the renin-angiotensin-aldosterone system, also known as the RAS. And I'll be honest, this one can be a little bit of a doozy. There are 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 AMP course, the renin-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 increased 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 going to 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 going to see renin, then angiotensin, and then aldosterone. So keep that in mind as we go through these. So first up, our blood pressure is going to decrease. We're going to have less blood flow to our kidneys, whatever happens. And then as a result of that, our macula densa cells will detect a low glomerular filtration rate because they're going to be receiving less sodium chloride. So our macula densa cells will then signal to our kidneys, hey, we have to release the enzyme renin into the bloodstream. So the kidneys release renin, and there is the first piece of our name. So then renin is going to go to the liver where it converts angiotensinogen into angiotensin 1. Angiotensin 1 will then travel to our lungs where it gets converted into angiotensin 2. And angiotensin 2 is going to be really the main player here. So there is the angiotensin piece of our name. And angiotensin 2 has widespread effects on the body in order to increase blood pressure. So it's going to be directly increasing blood pressure. It's going to be increasing blood volume, as well as having a direct effect on glomerular filtration pressure and rate. So it's going to be very busy. Now we're going to 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 going to 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 constricted it. You can imagine how the water coming out of it is going to be coming at a much higher pressure, and that's what's happening in your body there. But right off the bat, we have this increase in blood pressure as a result of that vasoconstriction. Now, moving over to this middle piece, we're also going to 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, angiotensin 2 increases blood volume in 2 ways. So we're going to start over here. And that angiotensin 2 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 the reabsorption of sodium, that is also going to cause the reabsorption of water by osmosis. We'll talk about this in some upcoming videos, but long story short, basically, water wants to follow high electrolyte 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 going to 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 2, we're going to move over here now, angiotensin 2 is also going to 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 going to have the exact same effect. It's going to 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 o

Renal Physiology: Regulation of Glomerular Filtration Example 5

Okay. So which of the following hormones is responsible for increasing the 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 I. Angiotensin I is not going to have any major effects. That's just going to need to get converted to angiotensin II. So that is definitely out. Now remember, angiotensin II 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. So angiotensin II is out.

B is aldosterone, and that one is correct. Remember those "d" sounds, aldosterone, distal tubule, collecting duct. They all kind of go together. So our answer here is 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 Aldosterone.

Angiotensin-II directly increases glomerular filtration pressure by _____________ the ___________ arteriole.

• A. Constricting; afferent.
• B. Constricting; efferent.
• C. Dilating; afferent.
• D. Dilating; efferent.

Here’s what students ask on this topic:

What is the myogenic mechanism in the regulation of glomerular filtration rate (GFR)?

The myogenic mechanism is an internal regulation technique where the kidneys engage in autoregulation to maintain a consistent glomerular filtration rate (GFR). This mechanism involves the afferent arteriole's response to changes in blood pressure. When systemic blood pressure increases, the afferent arteriole's smooth muscle stretches and contracts, reducing blood flow into the glomerulus and maintaining GFR. Conversely, when blood pressure decreases, the afferent arteriole relaxes, increasing blood flow into the glomerulus to keep GFR stable. This mechanism ensures that minor daily fluctuations in blood pressure do not significantly impact kidney function.

How does the tubuloglomerular feedback mechanism regulate GFR?

The tubuloglomerular feedback mechanism is another form of renal autoregulation that adjusts the afferent arteriole in response to changes in blood pressure. Macula densa cells in the renal tubule detect sodium chloride levels. When blood pressure increases, GFR and filtrate volume rise, leading to more sodium chloride reaching the macula densa cells. These cells release vasoconstrictor chemicals, causing the afferent arteriole to constrict and reduce GFR. Conversely, when blood pressure decreases, less sodium chloride reaches the macula densa cells, leading to the relaxation of the afferent arteriole and an increase in GFR. This mechanism helps fine-tune GFR in response to minor blood pressure changes.

What role does the renin-angiotensin-aldosterone system (RAAS) play in regulating GFR?

The renin-angiotensin-aldosterone system (RAAS) is an external regulation mechanism that responds to significant changes in blood pressure. When blood pressure drops, the kidneys release renin, which converts angiotensinogen to angiotensin I, and then to angiotensin II in the lungs. Angiotensin II causes systemic vasoconstriction, increasing blood pressure. It also promotes sodium reabsorption in the proximal tubule and distal tubule/collecting duct, increasing blood volume. Additionally, angiotensin II constricts the efferent arteriole, increasing glomerular filtration pressure and GFR. RAAS thus helps restore blood pressure and maintain GFR during significant physiological changes.

How does the neural mechanism affect glomerular filtration rate (GFR)?

The neural mechanism involves the sympathetic nervous system, which overrides renal autoregulation during fight-or-flight situations. Increased sympathetic activity releases norepinephrine, causing vasoconstriction of the afferent and efferent arterioles. This reduces blood flow into and out of the glomerulus, decreasing GFR. The primary purpose is to minimize fluid loss and preserve blood volume and pressure for vital organs during emergencies. This mechanism ensures that the body prioritizes essential functions over urine production in critical situations.

What is the relationship between arteriolar diameter and glomerular filtration rate (GFR)?

Arteriolar diameter directly affects glomerular filtration pressure and, consequently, the glomerular filtration rate (GFR). Vasoconstriction of the afferent arteriole reduces blood flow into the glomerulus, decreasing filtration pressure and GFR. Conversely, vasodilation of the afferent arteriole increases blood flow, raising filtration pressure and GFR. For the efferent arteriole, vasoconstriction causes blood to back up in the glomerulus, increasing filtration pressure and GFR, while vasodilation allows blood to exit more freely, reducing filtration pressure and GFR. These adjustments help maintain a stable GFR despite changes in systemic blood pressure.