Here. Let me set this up for you. So we have the afferent arteriole. I’d like for you to begin up there,
afferent arteriole. How did you give rise to this? It was a renal artery. And it came in, and what did it do?
Interlobar. What was next? Interlobular. What’s the name? Well, you have your arcuate.
And you had your Interlobular. What was another name for that? Cortical radiate.
And you have the afferent arteriole. And here we are. I want you to come towards the glomerulus.
You’re going to form a tuft of capillaries. I’ve mentioned that before. The afferent arteriole is coming in.
And you see all those structures there? That’s a lot of structures. Let me set each one up.
What's inside my afferent arteriole? I’m sorry. What? I didn't hear you. One more time. Good.
Plasma. Excellent. So your plasma coming through there. Good. Can you hear me? Loud and clear.
Afferent arteriole, plasma, filtering through. Tell me about hydrostatic pressure from physio.
Increased. It ensures filtration, right? Ensures filtration. Through what? Through the endothelial cells
across the basement membrane. Into where? Into the Bowman's space. Okay.
So now, tell me about the cells that we see in green. They're called juxtaglomerular cells.
What are they responsible for? They're responsible for measuring the pressure within the afferent
arteriole, aren't they? Mm-hmm. So let's say that you have decreased profusion to the kidney.
How did that occur? You tell me what the diagnosis is in older patient, male, approximately
52 years of age, blood pressure: 160 over 90, three different times on three different clinical visits
So far, diagnosis? Hypertension. We're not done. Now, you go ahead and check the kidney,
or excuse me, you auscultate the renal area, and you hear noise, bruit, your renal bruit.
Give me diagnosis. What's causing the hypertension? What’s causing the bruit?
A 52-year-old male, the bruit is caused by atherosclerosis. Where? Renal artery. Good?
What caused the 160 over 90? Secondary hypertension. Why? Ah, this will explain everything.
The renal artery has been cut off. Take a look at the previous slide if you need to so that you see
the positioning of the afferent versus renal artery, right? Now, you have decreased profusion
through the afferent. This is not good. You have decreased profusion. That kidney must maintain
GFR at all times. Tell me what the juxtaglomerular cells are going to release here
due to renal artery stenosis, secondary to atherosclerosis. Renin. Good. What’s the name
of that receptor that those JG cells have, JG, juxtaglomerular? Beta-1? What are they going to release?
Renin. Good. Continue the story. Renin, angiotensin II, aldosterone. What’s my blood pressure
in my 52-year-old male? 160 over 90. Was this primary or secondary hypertension?
Secondary hypertension, huh? Secondary hypertension. You got this? You better. You have no choice.
You have to know this. Next, what's on the other side? Well, the afferent arteriole with the JG cells
are going to communicate with a distal tubule. What’s in there? What’s in the distal tubule?
You wish it was me being flushed down the toilet. It’s not. It’s urine. That’s urine in the distal tubule.
You see it? Okay. Good. So that’s urine in the distal tubule. Ha! And what sense in the urine?
It’s not the juxtaglomerular cells. It’s the macula densa. Are we clear? So in physio, you did
a little bit of a reflex between the macula densa and the juxtaglomerular cells. Yeah, you did.
And that was called the tubuloglomerular feedback. We’ll get to it in due time. Not yet.
And the macula densa is sensing what? The sodium and chloride within the urine.
Are you putting all of these together? I hope so. I just gave you one example.
Now as we move, progress through here in this lecture series, we’re going to go ahead and talk about
the efferent arteriole in great detail. We’ll talk about the afferent arteriole in great detail.
We’ll bring all these structures together. We’re going to put in more and more and more pathologies.
It’ll be fun. Trust me. All we’re doing is laying down foundation. Are you having a good time?
Smile for me. Okay. So let’s take a look at this interesting graph. Quickly. It's called autoregulation.
Autoregulation, let me set this up for you. On the X axis is profusion. In other words, blood pressure.
On your Y axis is your tissue flow. Okay? Now, tell me about autoregulation that you learned of.
How important is that for a body? Really important. What do you mean? Autoregulation in the brain?
What does that do? It ensures that the brain receives enough oxygen at almost all times, right?
So as soon as you have any hypoxia, what are the cerebral blood vessels doing? Vasodilation, right?
What did I just say? As soon as the patient has hypoxia for five minutes, your neurons are going to die.
You can’t do that. So as soon as the body senses and the central chemoreceptors senses
the carbon dioxide, then what does the cerebral blood vessels do? Autoregulation, vasodilate.
What about the skeletal blood vessels when there's hypoxia? Vasodilate, right? What about the kidney?
This is all part of autoregulation. Very important in all the major organs, brain especially,
brain especially, brain especially. But you also have it taking place in the kidney as well.
And that’s what this entire graph is about. This green line that you’re seeing, you see where it says
the Y curve? Take a look at Y curve. Take a second here. Okay. Y represents perfect autoregulation.
How do you know? I want you to take a look at that line between point A and point B.
Take a look at the line between point A and point B. Is there any fluctuation there?
Perfectly horizontal. Tell me about the Y axis. What does that represent? Flow.
So the flow, did it change at all from A to B? No, it didn't. Point Y stayed the same.
How was that possible? So what did change between A to B from the green line or in general?
It’s the pressure. So go down to the X axis. A represents a perfusion pressure of 40.
B represents a perfusion pressure of 140. Wow! That’s a difference of 100 mm Hg.
And you're telling me, Dr. Raj, that between A to B, that there was no change in flow?
That’s exactly what I’m telling you. How did that occur? Autoregulation. So what does that mean to you?
There is no communication with the brain. There is a reflex in which it was able to handle the pressure
at the level of the kidney just like that, like a reflex. So now, this is autoregulation.
You pay attention. As the pressure starts dropping from 90, point C is normal.
Point C as in Charlie is 90. Let’s call that normal. As your pressure starts dropping
all the way down to 40, what do you expect your blood vessels to do so that you maintain proper flow?
A represents vasodilation, part of autoregulation so that the flow doesn’t diminish,
the pressure starts decreasing. But autoregulation causes vasodilation. That’s point A.
Whereas if you have point B, now what does that mean to you? Your pressure is increased.
Autoregulation tells your blood vessels to do what? Vasoconstrict, we have B.
We pretty much identified the perfect autoregulation points on this line for horizontal.
That is as far as I’m going to go with you on this. I need you to at least understand autoregulation
and its specifics. At any point in time, any one of your license exam could ask you about curve X
in which there is absolutely no autoregulation. And that dashed line represents mild autoregulation.
I’ll go as far as that. But your focus right now in pathology is going to be between A and B,
that green line exhibiting perfect, perfect autoregulation. Let’s move on.