General overview of the RAAS system: Cells and hormones | NCLEX-RN | Khan Academy


The body has a really,
really cool way of controlling blood pressure. And you’ll hear about
this RAAS system, and RAAS stands for
Renin-Angiotensin, R-A A- Aldosterone System. So let’s go through this RAAS
system, kind of as an overview, just looking at where things
start from and where things go, in terms of cells and hormones. So those are the
two things I want to try to distinguish between. So this RAAS system, R-A-A-S,
begins with a set of cells. So I’m going to
draw all of my cells as little blue houses like that. And the hormones
that they release are going to be
orange messengers. So I’m going to draw
a little messenger. This will be my little person. And so the person is the hormone
and the blue house is the cell. Now, the key cell in the RAAS
system is juxtaglomerular cell. It’s a JG cell. And these juxtaglomerular cells
are actually in the kidney, but they’re in a
specific location. They’re actually
in blood vessels. And if you look
closely, these JG cells are nothing more than very
special smooth muscle cells. So if you look in
the blood vessel they’re actually just
like smooth muscle cells. I’m going to write smooth
muscle just to remind you. This is just a reminder
of where they are. And of course, these
are in the kidney. So here’s my little kidney. It may not look like
a kidney but that’s what it’s supposed to be. So the juxtaglomerular
cells are releasing a hormone called renin. And when would they do that? Well, renin is
eventually– we’ll see when– eventually going to
help us raise blood pressure. So if the juxtaglomerular
cells, if these guys, notice that blood
pressure is low, that would be a trigger
for releasing renin. That’s the first trigger. So, low blood pressure. Very good. Now, that’s not
the only trigger. There are actually
three triggers in total. So let me write
out two and three, and let’s go through
what they are. So the second trigger
is a neighboring cell. So this neighboring cell is
actually a sympathetic nerve cell. And we know that
sympathetic nerve cells fire whenever something
big is going on. So for example, let’s say
you’re running away from a bear, or let’s say you’re
trying to win a fight, or let’s say you’re in a car
accident and you’re bleeding. Any sort of major,
major stressor is going to cause these
nerve cells to start firing. And when they fire, that JG
cell starts releasing renin. So the second trigger
would be sympathetics. I’ll just write sympathetics. Or maybe sympathetic nerves. Now, if these are your
neighboring cells, these little sympathetic nerve
cells, because they literally end right on the JG cells,
then a little ways away– still the kidney of course– but
still a little ways away, not touching the JG cells,
would be the macula densa cells. Now stay with me for this. These macula densa cells
are also in the kidney. And actually
they’re specifically in the distal tubule
of the nephron. So remember, the distal
convoluted tubule. They’re there. And their interesting ability
is the ability to sense sodium. And when you have low blood
pressure, not a lot of blood is moving through
that glomerulus, and so not a lot
of fluid is moving through the nephron as a result. And a lot of the salt
is being reabsorbed. So by the time it gets to
the distal convoluted tubule, the macula densa
cells, they’re kind of tasting or sensing
the fluid that goes by. And they say, there’s
not a lot of salt here. And they put two
and two together and they realize that the
reason there’s not a lot of salt is that blood pressure is low. So when they don’t sense
much salt they say, hey JG cells, wake up,
do something about this. Raise blood pressure for us. And so they send a message over
in the form of prostaglandins. So prostaglandins are
kind of local messengers. Unlike renin, which is kind
of a long distance messenger, prostaglandins act locally. And actually, lots and lots
of cells in our body use prostaglandins to
send local messages. So that’s what they do. So the third trigger,
just to summarize it, would be low salt in the
distal convoluted tubule. And you know, specifically,
that it’s the macula densa cells that pick up on this. OK. So these are the three major
triggers for renin release. And, now this is all happening
in the kidney, right? That’s where all this
action is occurring. But you know there are
other organs involved in blood pressure
control as well. And the one that is next on
our list is the liver cell. So liver cells are
actually– here we go, a little
house for cells– are also making a
hormone of their own. And it’s going to meet up
with renin in a second. And it’s called angiotensinogen. And angiotensinogen is
like a sleep-walker. If you were to zoom in on
its face it would be asleep. And so, I’m going
to draw it that way. It’s there and it’s
moving around the body but it’s not active, and
that’s the key thing. It’s not active. But it meets renin. And renin literally chops off
a big hunk of angiotensinogen. And if that doesn’t wake
you, I don’t know what would. So angiotensinogen
becomes angiotensin I after meeting renin. So renin is an enzyme
that cuts a big chunk of this angiotensinogen
protein away and angiotensin I is the result. And if you were to zoom
in on this guy’s face, it would be awake. Maybe even a little smile. So angiotensin I now floats
through blood vessels. And of course blood vessels
have cells lining them. So let’s draw a little house. So little cells, and these
are the endothelial cells. These are the cells that
are lining the blood vessel on the inside. And classically,
we used to think that this is almost always
happening in the lungs. But more and more, we’re
realizing that it definitely does happen in
the lungs but it’s in other places as well,
other vessels as well. And so endothelial cells, in
a number of parts of our body, including the lungs,
are able to convert angiotensin I into
angiotensin II. So angiotensin II is formed. And this is also, of
course, a hormone. So I’ll draw it as
a little person. And angiotensin II
is happy as a clam, because angiotensin II
has lots of activity. A very, very active hormone. It does all sorts of things. And I’m going to draw
them in for you now. So angiotensin II will go out
to a number of different places. I’m going to draw
four arrowheads here. One, two, and then two
in the middle here. Three, let’s do four. As it goes to four places. And four different cell types
are affected by angiotensin II. Now keep in mind at the
beginning of all this, we’re trying to
raise blood pressure. So just keep that
thought in your head. So four different cell
types are affected and here is the fourth. So the first one over here
is smooth muscle cells in the blood vessels. And this is blood vessels
all over the body, not just in the kidney, but
this is smooth muscle cells all over the body,
are going to contract. They’re going to
constrict down and they’re going to cause
increased resistance. Because you remember that as
the blood vessels constrict, vasoconstrict, that will
increase resistance. OK. So that’s one effect. Now in a different
cell type altogether, in the kidney
cells, you actually have the ability– the
angiotensin II actually makes these kidney cells
hold on to more water. So you have more volume. It actually helps the kidney
hold on to more water. And more volume, think about
in terms of stroke volume, is going to increase
stroke volume. So you’ve got
increased resistance, and now increased stroke volume. So those are two cell types
that angiotensin II will act on. It also acts on a
couple of glands. I’m going to try to draw
for you the pituitary gland. And this pituitary
gland is sitting at the base of the brain. And this gland is called that
because it secretes hormones, as well. So it’s actually sending
off messengers, as well. So here’s a little
hormone again in orange. Remember, all our
hormones are orange. And this one is called ADH. ADH, or antidiuretic hormone. And that ADH does some
of the same stuff, at the end of the day, that
angiotensin II will do, in that it will increase
resistance of blood vessels. And it will actually,
also, increase volume by making the kidney
hold onto more water. Now, the fourth cell type is
going to be the adrenal gland. So the adrenal gland is here. And this adrenal
is called ad-renal because it’s sitting on
top of the kidney, which is the adrenal. This adrenal gland is
also making a hormone, because it’s a gland,
and that hormone is going to act right there. And this is their
little messenger, and this is called aldosterone. So you’ve got
aldosterone and ADH that are also acting on
some of the same cells. And I should rephrase that. Not exactly the same
cells, but the same organs as the angiotensin II. So here, aldosterone is
going to act on kidney cells to increase volume. And ADH is going to act
on, as I said before, the kidney and smooth muscle. So let me scroll up
and show you now, from the top, some interesting
things I want to point out. So we’ve got, at the very
top, all of the action, you’ll remember, started
in our kidneys, right? It started in the kidney, or the
macula densa cell, and our JG cell, and even our nerve
endings were in the kidneys. And one of the key
target organs down here is, of course, the kidneys. So things are
starting in the kidney and also ending in the kidney. Now you’ll say, well, what
about the smooth muscle cells and that,
all over the body? And you’re absolutely right. It does also affect
smooth muscle in other parts of the body. But I just want to
point out the fact that the kidney is a
major player in this game. Now that’s one point. The other point is
that when people talk about the
renin-angiotensin-aldosterone system, they’re talking
about certain pathways. And they’re specifically
talking about, for example, this arrow right here,
this hormone obviously. And they’re talking about
this angiotensinogen and they’re talking
about angiotensin I. And they’re also referring
to angiotensin II, and all of its targets. So they’re going to talk
about angiotensin II affecting the smooth muscle,
and the two glands, the pituitary, as well
as the adrenal gland, and its effect on the kidney. So they’re really referring
to all of those things. So they want to make sure you
remember that it’s affecting four, at least four,
target cell types. And finally, that
aldosterone down here has a huge effect on
the kidney, as well. So these are the
important points to take away from this
overview, that there are many different
hormones involved– and I’ve tried to
keep them color coded all in orange to make sure
we keep track of them– and the fact that the kidney
is a major player in blood pressure control.

81 thoughts on “General overview of the RAAS system: Cells and hormones | NCLEX-RN | Khan Academy

  1. 1. Yes, Going from A1 to A2 requires ACE
    2. A2 has effects on the Prox. Conv. Tubule to reabsorb Na+ (this is not negligible)
    3. Hypervolemia with Hyponatremia sounds like an SIADH type syndrome. In SIADH, GFR is high, so Renin levels are low. We will be doing an ANP video in the future to help describe its role.

  2. doesn't your SV decrease when the kidney holds more water, which doesn't get absorbed by the capillaries, which also doesn't increase blood volume?

  3. there other things that control bp ,ANP that is activated when bp is rised and there is hypernatemia/elivation of Na ion and then the ANP on right atria is activated and acts on the collactnig tube of the kidney and leads excration of Na and retenssion of Ka,2 the prostaglandin ,nitric oxid and so on

  4. Your video's really helped me! One thing I would like to ask is… could you sometimes write bigger letters please?:) Your " smooth muscle" was a challenge to read 🙂
    Thank a lot!

  5. thanks for the tutorial it was very helpful, does this mean Hypertension is also responsible for the urine output of a person?

  6. Thanks for the great teaching. I'm not sure why the last three people who commented were on an education site. Keep up the great work! 

  7. Thanks for the information. This was a great refresher.  Not only did it brush me up on my knowledge of the RASS, it also touched on the action of ACE Inhibitors and Vasopressin.  Great job

  8. I really enjoy your videos, actually I think out of all khanacademy videos, yours are the best.  You really make a lot of sense of things and help consolidate the info in my head.  You really gave me a chuckle with your angiotensinogen face in this video.

  9. You are the BEST! You are helping me get through graduate school. You don't talk too fast, you break things down and make them fun, interesting and understandable. Also you have an amazingly great voice! Thank you so much for your videos

  10. could you please explain to me,how sympathetic nerves can increase renin secretion?could you please give me the link or reference for more clarification?

  11. 4:06 … how does less BP lead to less movement of fluid ? does filtration rate increase or decrease ? how ?

  12. could you please tell me ,so this Renin Angiostensin Aldosteron System is for activated renin angiostensin and aldosteron ,for example when that little guy ( renin ) knows that blood pressure is low ?so the renin have to activated for raise the blood pressure

  13. Could you explain me what makes the Sympathetic Nerve fire when the pressure drops? PRessoreceptors, or B-Receptors?

  14. I find it strange that ACE was never mentioned in this vid (especially due to clinical significance), but still a great overview. Loving the khan academy medicine videos as introductions to topics/study motivators. Thank you 👍🏼

  15. Nursing student here, struggling in Pathophisiology and your videos are SO CRAZY HELPFUL!!! My peers love them too. Can't thank you enough!

  16. I'm a little confused about what actually induces renin secretion. Other than sympathetic innervation, you also mention a drop in blood pressure as well as a drop in Sodium concentration (in tubule fluid or in blood? Not necessarily the same thing). I have read that the decrease in blood pressure is actually detected by baroreceptors in the afferent arteriols in the kidney, not by the JG cells. Does anyone know?

    Also, I have read that the macula densa detects a decrease in sodium as you say, but also a decrease in blood perfusion to the kidney. Both of these factors will induce Renin-secretion. Does anyone know about this blood perfusion to the macula densa thing? Or is it just misinterpreted to the drop in blood pressure?

  17. "CHOPS OFF A BIG HUNK! and if that doesn't wake you up, I don't know what will."

    Funny thing is that I was laying in bed, all comfy, my eyes closed, just about to drift off into dreamland, and that woke me the heck up thank you very much

  18. Excellent video and very thorough, but it's missing angiotensin converting enzyme! So important for us nursing students when considering the effects of ACE inhibitors.

  19. For everyone wondering about ACE (Angiotensin Converting Enzym), its on the surface of the Endothlial cells which he describes at 7:20. Or you can kinda say that ACE is released by Endothelial cells but they are still attatched to the walls of the vessels.

  20. constructive critic: I think it is better to paint as realistic as possible, not small people smiley faces etc. Painting skills is something everyone can learn. The more realistic it is, the better understanding as well you get an idea how it actually looks like. Great voice, just the paintings that makes me confused… I might not be the only one.

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