>>Dr. Ketchum: Okay, then we have tubular secretion next. So we’re switching gears,
now we’re secreting. So now we’re looking at solutes that were not filtered at the glomerulus.
So let’s use green again here. You have plasma that comes in the afferent arteriole
into the glomerulus, but it does not get filtered. It goes back to the efferent arteriole. Then
it’s passing into the peritubular capillaries, and it’s on its way back to the heart. But
lo and behold, woah, some of it gets secreted into the lumen of the nephron, okay? The tubule.
So what gets secreted? Hydrogen ions are going to get secreted, and remember, we already
talked about their secretion in the proximal tubule. So now we’re going to talk about
their secretion in the distal and collecting tubules as well. Potassium ions are also going
to be secreted. And this is controlled, so it’s controlled by aldosterone. And then
we have some organic anions and cations as well. Okay, so let’s focus on potassium
here for a moment. So once again, we’re going to start where we always do—
basolateral membrane here. And so we have number one, which is our primary active transport.
So we know that sodium is at a low concentration and potassium’s at a high concentration
inside of our cell. So potassium’s at a low concentration out here in the interstitial
fluid.
Okay, so we want to reabsorb it. So let’s start out in the plasma. In the plasma, we
have a high concentration of potassium. So potassium’s diffusing through, remember,
the pores between the endothelial cells in the capillary? Potassium diffuses through
from a high concentration toward a lower concentration, then we pump it in using primary active transport.
Then it goes through a channel on the apical membrane. So this is the apical membrane,
and because it’s going through a channel and because it’s going from a high concentration
to a low concentration, that’s called facilitated diffusion.
Okay, so—so now what we’ve done is we’ve talked about potassium reabsorption and the
proximal convoluted tubule. We’ve also talked about potassium secretion, which is what we’ve
just now done in the distal convoluted tubule and the collecting ducts. Okay, so we’re
reabsorbing and we’re secreting potassium. It’s a little bit odd, right? So think about
the net effect of these. We are going to reabsorb more potassium than what gets secreted. Let’s
take a look at how that’s going to happen.
So in this flowchart, you guys are already very familiar with the renin-angiotensin system,
and that’s what part of this is—or all of it, actually. It’s just a very condensed
version. So when you have low salt, low extracellular fluid volume, and low blood pressure, then
that’s going to end up simulating your sympathetic response. And the sympathetic response is
going to wind up, causing the release of renin. Remember renin is an enzyme, just to give
you a quick review. And it’s an enzyme synthesized and secreted by the kidneys under the direction
of the sympathetic nervous system. So that’s going to wind up, causing the production of
angiotensin one, which ends up causing that to get converted to angiotensin two. And angiotensin
two then stimulates the zona glomerulosa of the adrenal cortex. And that, then, is going
to cause aldosterone release.
Okay, so the other thing that causes aldosterone release are looking at the levels of potassium,
as well as sodium levels. Okay, that’s something else that can cause the synthesis or secretion
of aldosterone. If you have low sodium plasma, right, or high potassium plasma, we talked
about this when we talked about chapter six—those can both stimulate aldosterone release as
well. So you’re not solely dependent on the sympathetic or the renin-angiotensin system
to release aldosterone. Remember that these controls here—low sodium, high potassium—remember
that this is a humoral control, so aldosterone is being released based on the needs of the
plasma.
Okay, so once aldosterone gets released, aldosterone then is going to increase the number of sodium-potassium
pumps on the basolateral membrane. So the more pumps you have, the more ions you can
move, right? Then aldosterone is also going to increase the number of sodium and potassium
channels on the apical membrane. More potassium channels you have, the more potassium secretion
you can do. The more sodium channels you have, the more sodium reabsorption you can do, which
is what’s illustrated in this flow chart, okay? The more potassium that you secrete,
the more that’s going to get excreted. The more sodium that you reabsorb, the less sodium
that’s going to be excreted, okay? So be sure you understand that terminology.
Okay, so the next slide then, this gives you a really nice indication of how aldosterone
is actually functioning. So here’s aldosterone in the plasma, and you already know how it
got there. And so it’s going to diffuse into the ep—the cytoplasm of the distal
convoluted tubule or the collecting duct, and it’s going to bind to a receptor. So
remember when this happens. So here’s your ligand as aldosterone, it binds to this receptor.
And remember, you form a hormone receptor complex, which binds to the hormone response
element on the DNA, and then ultimately, you activate a gene. And once you activate that gene
then transcription and translation can take place, and you make protein. So the protein
that you’re making are these carrier proteins, right? So if you’re going to be putting
more sodium-potassium pumps on the basolateral membrane, you better be making protein, right,
because you need pumps. And then the same is true for the apical membrane—you’ve
got to make these channels. These are proteins, every single one of these. So you’ve got
to activate the gene in order to make those proteins. Okay, so I think that ties in chapter
five really nicely and brings you back to those in—intracellular mediated responses.