 Aldosterone is a little bit more complicated. So first of all, aldosterone is a steroid hormone. It's produced in the adrenal cortex as opposed to the adrenal medulla. So remember that I drew you at one point, one time, I drew you an adrenal gland. And I showed you the adrenal medulla, and this was where the sympathetic portion of the adrenal gland came into play. Remember, we had the ganglion cells are actually found in the adrenal medulla. So the adrenal medulla is actually nervous tissue, and that's where basically we dump epinephrine and norepinephrine directly into the bloodstream. So I'm giving you context for what you already know about the adrenal glands. Well, aldosterone is going to be produced in the cortex. There are other hormones, steroid hormones, that are produced in the adrenal cortex. I think it's relevant to take a second and go, dude, why? Who tells the adrenal cortex to produce aldosterone? And I'm going to take you somewhere to show you who does it. Hopefully this doesn't scare you. Hopefully this just makes you go, oh, yeah. Right? Are you going, oh, yeah, right now? Oh, yeah. This was from our first kidney lecture where we talked about the macula densa cells in the distal convoluted tubule or ascending loop of Henle that are in contact with the juxtaglomerular cells found on the afferent and efferent arterioles. Remember that? And we talked about how the macula densa cells actually monitor the filtrate. Well, the idea is that the macula densa cells detect low sodium, which indicates low blood pressure. We have low blood pressure. And so basically with low blood pressure, you have low glomerular filtration rate, which leaves more time for filtrate to hang out in the nephron and have the sodium removed from it. And so if you get to this point in the nephron and there's a low sodium concentration, then we're going to send a message, dude, something's funky here. So let's produce renin, which activates angiotensinogen, turns it into angiotensin I, which is acted upon by ACE and turned into angiotensin II. Remember, angiotensin II was the one that was like, dude, let's get blood pressure up. Let's vasoconstrict. You got to be thirsty. Let's increase cardiac output. All of that together is going to increase blood pressure, which the idea is to return glomerular filtration rate back to normal. Well, something else that happens that we didn't talk about is that I can't decide which color to make it. The fourth thing that angiotensin II does is it increases aldosterone production. So if you have low blood pressure, one of the responses is to produce aldosterone. Now, there is nothing simple about this. In fact, one of the textbooks that I was reading just said that this is one of the most complicated interactive pathways in the body. So if you're feeling like, whoa, this is crazy, it is, and it isn't linear. It's very net-like. But let's look at what aldosterone does. We now know that angiotensin II is going to come in and act on the adrenal cortex and result in the production or the dumping of aldosterone into the blood. So I'm just going to do our normal little picture. I'm going to try to give myself a little bit more space to do this. But here's a blood vessel. And I'm just going to go, dude, how about some aldosterone? Here's a little aldosterone molecule. Who put it in the blood? The adrenal cortex. Why did they put it in the blood? Angiotensin II told it to. Who made angiotensin II? We were having low blood pressure issues, glomerular filtration rate, our juxtaglomerular apparatus took matters into its own hands and requested some aldosterone production. Good. Well, aldosterone can act. This is my giant cell, tubule cell. This can be in the distal convoluted tubule or the collecting duct. There are multiple different kinds of cells in the collecting duct. Some of them function in pH homeostasis. These kinds of cells, they're called principal cells. These guys are sensitive. They have receptors that are sensitive to aldosterone. Now, aldosterone is a steroid hormone. So it's going to diffuse directly through the cell membrane and it's going to come in contact with cytoplasmic receptors. So the receptors aren't on the cell membrane. Now, you remember steroid hormone. What does steroid hormone cause to happen? Protein synthesis, that's protein synthesis. Protein synthesis. And I'm going to tell you I've got a list of the things that are going to be protein synthesized. Thank you very much, aldosterone. One of them is, I think I always do sodium channels. Another one is potassium channels. Interesting. The protein synthesis results, thanks to aldosterone, results in the production of sodium channels and potassium channels that get embedded in the luminal membrane of the distal convoluted tubule or the collecting duct. Are you cool? You know what else happens? This kind of makes sense. My friends, who's this? The sodium potassium pump. We are going to throw some extra sodium potassium pumps in. We are going to increase the activity of the sodium potassium pumps. Sodium potassium pump is going to do what it always does. It's going to pump sodium. We have a better color green than that. It's going to pump sodium out. Dude, what just happened to sodium? Went into the bloodstream. Fantastic. It's also going to pump who in? Yeah, this is a weird part. It's going to pump potassium in. This is totally normal. Of course it is. If we're pumping sodium out, what did we just create inside the collecting duct principle cell? We created a sodium gradient. And so sodium, oops, we got to go with the green. Sodium in the filtrate is going to come in. And because we activated more sodium potassium pumps, we are going to functionally reabsorb sodium from the filtrate into the bloodstream. Does that work for everybody? However, we have this excess of potassium. What are we going to do with that? One of the side effects of aldosterone is potassium secretion. Not like massive, let's dump, let's filter. We're not filtering. We are specifically dumping potassium into the filtrate. So this is interesting because the potassium, where did it come from? It had to have come from the blood. When aldosterone goes into action, it's going to increase sodium concentration, but it's going to decrease potassium concentration. And that can be a problem. If you have potassium issues, then looking at aldosterone function might be something that you need to do. Now, most of the time, aldosterone doesn't act alone. If we're reabsorbing sodium, most of the time we also have vasopressin or anti-diuretic hormone acting at the same time. So that's also going to pull water in to the mix. All right, that seemed a little bit straightforward, pH is a little scary, but I think that was pretty straightforward, wasn't it? Easy, peasy. Now, let's talk about pH. pH homeostasis overall.