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.
