In contrast, increases of plasma potassium directly stimulate aldosterone secretion. This effect of potassium on aldosterone serves as a protective mechanism against the development of hyperkalemia.
Conversely, hypokalemia inhibits aldosterone production. I'm going to draw it here. And the gland is actually called the adrenal gland. And this gland literally sits right on top of the kidney. And so let me draw the kidney here for you so you can kind of orient yourself to where this gland would be sitting. And, of course, you have two kidneys. And you have two adrenal glands. You have the left and the right. And if you were to look inside of the adrenal gland, you'd notice that, actually, in the middle of the adrenal gland is an area that looks different than the outside.
And we call that the medulla. The inside is the medulla. And the outer bit is the cortex. And they make different hormones. And this cortex is actually the part of the adrenal gland that makes the aldosterone.
So let me draw some cortex cells here for you. And in the middle is a blood vessel kind of running through. I'll draw that in just a moment.
So these cortex cells are basically like any other cells. They need food, they need nutrients, they need oxygen. And so these capillaries that are running through are going to provide all of that to these cortex cells. And if you were to take a microscope and, let's say, look deep within these cells. Maybe not even with a microscope, but let's say you were able to look deep within these cells, you'd notice that there is cholesterol in these cells.
So there's cholesterol sitting inside of the cells. Actually, not visible, but it is there. And the cholesterol, I've always wondered, what is the point of cholesterol?
It always seems like it's a bad thing. This cholesterol is actually really useful to these cells because it helps them make the hormone aldosterone. Actually, aldosterone comes from cholesterol.
And if you put the molecules next to each other, you'll see how similar they are. They actually look really, really similar. So these cells are the ones making aldosterone. But, of course, you can't just make aldosterone willy-nilly, you have to wait for the right moment, right? So when does that cell know to make aldosterone? What are the triggers? Well, there are a couple triggers. One would be if you see, or if those cells encounter angiotensin II.
So if angiotensin II comes around, that would be one of the triggers to let the cholesterol turn into aldosterone. Angiotensin II, you remember is floating through the body. It's actually quite a journey of its own, making its way from the liver initially and all the way into meeting renin and then meeting angiotensin converting enzyme.
So this angiotensin II has been around a long time and it finally makes its way to the cortex of the adrenal gland. And it is one of two stimulus for making aldosterone. And the other stimulus is actually not a hormone, but it's actually the ion potassium. So you know blood has a lot of sodium in it, but it also has a little bit of potassium in it. And if those potassium levels start creeping up, if you have a little bit too much potassium, then that is a stimulus for getting some aldosterone out there in the blood.
So these are the two triggers for getting cholesterol into aldosterone. So just keep that in mind. And let's actually now make a little space on our canvas and see exactly where the aldosterone works and how it works. How is aldosterone controlled? What happens if I have too much aldosterone? What happens if I have too little aldosterone? Last reviewed: Jan Prev. Adrenocorticotropic hormone. Related Endocrine Conditions.
Addison's disease Congenital adrenal hyperplasia Primary hyperaldosteronism View all Endocrine conditions. His muscle weakness gradually improved over the clinical course. The mild watery diarrhea also gradually improved, and he was able to intake orally. There are 3 important factors that affect renal potassium excretion: 1 increased mineralocorticoid receptor MR stimulation, 2 increased distal sodium delivery, and 3 increased nonreabsorbable ions in distal nephrons [ 1 ].
Metabolic alkalosis also was seen in this patient, which is usually associated with potassium loss from the upper gastrointestinal tract, such as with vomiting or nasogastric drainage, and is not usually seen with diarrhea or laxative abuse. The pathophysiology of metabolic alkalosis consists mainly of 2 parts: 1 loss of hydrogen and 2 increase of bicarbonate. The primary causes of the maintenance of metabolic alkalosis include 1 reduction of effective circulating volume, 2 chloride deficiency, 3 hypokalemia, and 4 decreased renal function [ 3 — 5 ].
In the present case, the main cause of metabolic alkalosis may have been volume depletion or chloride deficiency. In the present case, the kidneys seemed to be responding to hypokalemia normally based on the low PAC.
However, because the patient simultaneously showed volume depletion, the renin-angiotensin-aldosterone system RAAS should have been upregulated in order to maintain body fluid status.
Generally, when aldosterone increases, serum potassium decreases, because it promotes secretion in the distal tubules. In , through a study of hemodialysis patients, Henrich et al. There were two different dialysis protocols. In another group of 12 dialyses involving 8 patients including the original 5 patients , decreases in the plasma potassium level were permitted. In both groups, the goal was weight loss by ultrafiltration and all patients lost at least 0.
However, this study did not address the mechanism of aldosterone response. In addition, the mechanism of aldosterone response in conditions with both volume depletion and hypokalemia remains unclear.
The ability of aldosterone to signal the kidneys to stimulate sodium retention without potassium secretion in volume depletion and to stimulate potassium secretion without sodium retention in hyperkalemia has been referred to as the aldosterone paradox [ 7 ]. In , Shibata et al. There are mainly 2 types of cells in the renal collecting ducts: principal cells and intercalated cells.
The epithelial sodium channel and renal outer medullary potassium channel are expressed in the apical membrane of principal cells. Interestingly, MRs are expressed in all cells, but serine is phosphorylated only in MRs in intercalated cells.
Thus, in addition to MR signaling in principal cells, ANG2 signaling reduces phosphorylated serine , resulting in MR signaling activation in intercalated cells. The increase in chloride reabsorption results in a lumen with neutral potential, which prevents increased potassium efflux [ 8 ] Figure 2 a.
Moreover, several clinically relevant hormones stimulate sodium reabsorption in the initial part of the distal convoluted tubules DCT1 by increasing thiazide-sensitive NaCl cotransporter NCC activity. One of these hormones is ANG2 [ 9 , 10 ] Figure 2 a. Though the action of aldosterone remains controversial Figure 2 a , it would be possible for PAC to increase and for urinary sodium and chloride to decrease. This might have made the pathophysiology more complicated because they may have affected the response of the RAAS.
As a result, urinary sodium and chloride exhibited much higher levels than expected in this patient Figure 2 b. Meanwhile, urinary potassium was normally suppressed, probably due to both low PAC and volume depletion.
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