Aldosterone raises blood pressure and lowers potassium | NCLEX-RN | Khan Academy

Aldosterone raises blood pressure and lowers potassium | NCLEX-RN | Khan Academy

All right, we’ve
talked about renin, we’ve talked about angiotensin. Let’s talk about
aldosterone now. Aldosterone is the
final hormone that gets your blood
pressure to go up. And so where does it come from? Aldosterone comes from a gland. 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. So let me scroll down. And let’s go back. Let’s think back to our blood
vessel that enters the kidney. And we know that we call
that the afferent arteriole and it goes into the
glomerulus, which is that little clump of blood
vessels I just drew there. And the afferent arteriole
and efferent arteriole, this is all review now,
right, are in the kidney. These are the blood
vessels that have entered, and the efferent
arteriole is exiting the glomerulus of the kidney. And remember, this is our
little kidney nephron. The Bowman’s capsule, and the
proximal convoluted tubule, and we have that Loop of Henle. And we have that distal
convoluted tubule that goes like that. And then it all kind
of comes together in the collecting duct. So this is the nephron, right? This is our image
of the nephron. And now to answer the question
of where does aldosterone work, I needed to draw this
because I wanted to show you that it actually works in this
area that I’m circling in blue. So this is kind of the area that
the aldosterone is working on. And right here, this
part right here, is the late part of
the distal– so I’ll call it the late distal
convoluted tubule. And the other part that
it works on right here, is the collecting duct. So these are the two areas that
the aldosterone is actually going to have an effect on. So it’s going to
affect the kidneys. And it’s actually going
to also effect the gut, but I’m not going to get
into that too much detail because the main effect of
aldosterone is on the kidney. And so let’s try to blow
up some of these areas so you can see
exactly what I mean. Let me draw a cell here. Here’s one cell. And just imagine that you’ve
got another cell there and another cell there. And you’ve got, let’s
say, a few cells there. And they’re lining
the nephron, right? They’re lining the, let’s say,
the distal convoluted tubular, or the collecting duct. And these are called
principal cells. And it’s actually
spelled the way that a principal at a school
would be called or spelled. So this is a principal cell. And on the other side
of it, over here, you’ve got blood flowing. And you remember we talked about
the peritubular capillaries? Well, this is where
it comes into play. Peritubular capillary
is actually sitting next to the principal cell, and
blood is flowing through here. And, of course,
this is filtrate. Or what will soon be urine,
is flowing through here. So we’ve got blood and
urine flowing through. And we’ve got a couple
of surfaces here, right? So we’ve got one surface here. And this is called the
basolateral surface. And this becomes
really important because the surfaces
are where ions are going to be
dancing back and forth. And this is the other surface,
this is the apical surface. So this is the surface
between the principal cell and the filtrate, or the urine. OK, so we’ve got a couple
surfaces, we’ve got a cell, and we’ve got some
blood and urine. And now you remember that most
of the inside of the cells is going to be loaded
with potassium, right? So there’s a lot of
potassium in here. And if this is another
principal cell, there’s more potassium in here. And the blood is going
to have a lot of sodium. So let me draw sodium over here. So a lot of sodium in the blood. That’s the main solute. And a lot of potassium
in the cells. And now these aren’t the
only ions in the blood or in the cells. These are the main ion
in the blood and cells. So just keep that in mind. They’re not the only ones, but
they are the dominant ones. And so what happens
is that the cells want to maintain this
gradient, right? This is always the case. They always try to
maintain this gradient. And they have this wonderful
sodium potassium pump to do it, right? They have this
pump that basically gets two potassiums over here,
and it squeezes three sodiums out over here. Right? So we have this
sodium potassium pump. Three sodiums. And this pump does not
come for free, right? Because it takes energy to get
things to go in a direction they don’t want to go. So this is actually going to
take ATP to drive that pump. So now so far, I haven’t
actually mentioned aldosterone. Where does aldosterone work? Where we know it works
in the principal cell, but what does it do
in the cell, exactly? Well, it does three things, OK? So three things. One, let me write
it really clearly, is that it drives that sodium
potassium pump to work harder. OK. So it basically is going to get
even more potassium in the cell and even more sodium
over into the blood. So far so good, right? Second thing it does is it puts
in little potassium channels here. Well, that’s
interesting because we know that the cell’s got
a lot of potassium in it already, right? So if you have a
potassium channel, if that’s the second thing that
aldosterone does, number two, what do you think
is going to happen with that potassium in the cell? Where’s it going to go? Well, it’s going to
see that channel, and it’s going to say,
well, I’m out of here. I’m going to go into that urine. Because there’s a lot of
potassium in the cell already, and it wants to get over to a
place where there’s less of it. So it’s going to go
over to the urine side. So potassium’s going
to leave the cell. Well, that makes
it easier for that pump to work harder
because now it’s going to squeeze even more
potassium into the cell, right? This is going to
work even harder to get potassium in there. Because this potassium
is leaving and getting into the urine. So, really, at the
end of the day, what happens is that the blood– I’m
going to write it over here– kind of the net effect,
the blood is going to, one, it’s going to lose
potassium, right? Aldosterone is going to make
the blood lose potassium. And that makes perfect
sense because keep in mind one of the triggers for
aldosterone was high potassium. So this is a perfect
kind of system to now lower your potassium. It’s a nice little loop
that you’ve created, right? More potassium? No problem, make some
aldosterone, and aldosterone is going to help you lose
some of that potassium. OK, now going back
to aldosterone, what’s another
thing that it does? Well, it does this. It puts in little
sodium channels. This is a third
thing that it does. Now, if you have a
little sodium channel, let’s try to think
through what would happen. Sodium is going to make its
way into this cell, right? Because it’s going
to say, well, there’s not much sodium in there, so
I might move into the cell. So sodium gets into the cell. And then again, that sodium
potassium pump says, aha, sodium in the cell? , Great,
let’s pump it into the blood. So it’s actually going
to move from the cell over into the blood, and that
ATP is going to be used up, so it definitely takes
energy to do this. But at the end of
the day, you’re going to move sodium
from the urine– what would have been
urine– to the blood. So another effect,
another key effect is gain of sodium in the blood. And think through this. Now if I said at the beginning
that the main solute in blood is sodium, right? That’s the main way that
it’s attracting water through osmosis. And now you have more of it,
you have more sodium, well, then water is going to also get
pulled into the blood, right? It’s going to get pulled
into the blood as well. And so this is the other
key thing that happens. You gain sodium and water. And this is important
because, remember, the renin angiotensin
aldosterone system, the whole
point of it was to raise your blood pressure. Well, now you can
see how it actually works because the aldosterone
is going to pull in more sodium into the blood, and
then water’s going to follow, and all of this stuff
is going to lead to increased volume or
increased stroke volume. And remember, stroke volume
relates back to blood pressure. And therefore, blood pressure. So this is how
aldosterone works. It allows you to
drop your potassium. It allows you to
raise your sodium. The sodium pulls in some
water, and the water helps you raise your
blood pressure because of extra stroke volume. So let’s pause right there. We’ll pick up with
some more stuff that aldosterone does
in the next video.

57 Replies to “Aldosterone raises blood pressure and lowers potassium | NCLEX-RN | Khan Academy”

  1. Yes Aldosterone is made at some baseline level throughout the day, and that that level of production seems to go up and down based on the level of RAAS stimulation, Potassium levels, and even the time of day.

  2. i love your videos!! i'm a visual learner and i do like to know my stuff lol. reading only lasts me so long before i go crazy… -nclex test taker (soon i hope) haha

  3. that explains why we use potassium sparing diuretics for the prevention of potassium loss. Blocking the action of aldosterone you can get diuresis without K+ leaving. The downside is that it can drive to metabolic acidosis, giving that aldosterone stimulates H+ secretion.

  4. Your videos are absolutely amazing! I am currently taking anatomy and physiology 2 and I am struggling a great deal. My teacher is very nice but this is overall a very tough subject and you do an amazing job explaining it all!!! Do you do all the videos? Also, do you do videos upon request?

  5. wait….what about hydrogen….aldosterone also plays imp role in hydrogen secretion….promoting metabolic alkalosis…..
    btw great fan of ur videoa…jus clear the potassium bit plzzz

  6. Constantly high sodium causes high blood pressure since more water is retained in the blood to keep the osmolarity of the blood at its normal concentration

  7. I finally understand why my Addison's disease gives me metabolic acidosis when I go into crisis. I wondered if it was caused by the dyspnea, but it must be the opposite. Great lectures!

  8. I'm a M.D. physician in Mississippi and some of these lectures have helped me in revising what had gotten rusty in my brain.

  9. OMG! studying for my physio exam and this helped soooo much! I couldn't get the mechanism of aldosterone and its relation to K+ excretion.

  10. I really love your videos! I started learning hormones in school, but I wanted more detail. Then I found your channel! It's really helping out, so please continue working well. Thanks😂

  11. Hi, your videos are really really good and I find it really easy to
    understand. The most common exam question asked for Mpharm students is
    how does the loop diuretics affect the renal system. Ive searched it but
    its still not answering the question. Please help.

  12. Thank you. Your videos complement RN Sarah and my brilliant lecturer. I hope I can pass my exam on 25th May

  13. The theory doesn't stack up.
    How come some patients suffering from excess aldosterone i..e primary aldosteronimism doesn't exhibit low blood potassium levels?
    If excess sodium in blood raises blood pressure, why is that water tablets that depletes sodium has little to no effect on those suffering from primary aldosteronism?

  14. I need help my bp is over 200 🙁 was given hydralazine
    But other bp meds make me sick
    Working out knocks it down to 130 but it keeps going up and my heart hurts
    Stomach burns
    Bowel movements are fluid
    I drink coconut water
    Eat bananas and soup
    I can't take what my naturopath gave me iodine because I've been throwing it up I feel great on vitamin bs 👍🙂🙏Thank you so much for this video 🙏❤️❤️❤️❤️❤️

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