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MCAT
Course: MCAT > Unit 7
Lesson 13: Renal regulation of blood pressure- Renal regulation of blood pressure questions
- General overview of the RAAS system: Cells and hormones
- Renin production in the kidneys
- Activating angiotensin 2
- Angiotensin 2 raises blood pressure
- Aldosterone raises blood pressure and lowers potassium
- Aldosterone removes acid from the blood
- ADH secretion
- ADH effects on blood pressure
- Aldosterone and ADH
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ADH secretion
Learn the key triggers for ADH secretion. Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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- What does the optic chiasm do? Is it in any way relevant to ADH production or release?(6 votes)
- Luminoustedium is right. They aren't really related, but they just happen to sit near each other in the brain. The interesting thing is that if you get a pituitary tumor, the enlarged gland can press on the optic nerve and cause partial blindness. The type of blindness is called "bitemporal hemianopsia", which means that you lose sight in the outside portion of your vision in both eyes.(15 votes)
- Atthere is the whole picture of the Hypothalamus. He said ADH is made there. In class, I learned that ADH made the kidneys stop releasing more water. The hypothalamus made the RH hormone and send it to the Hypofyse. The hypofyse will produce ADH. This is what I learned in class on school. I hope I am clear above but I am confused. I hope someone can explain me where I am wrong. 4:17(3 votes)
- ADH is made in hypothalamus and then stored in the posterior pituitary gland. You are correct when you say that ADH acts on the kidneys to decrease water excretion (thereby increasing the amount of water in the blood, which increases stroke volume, which increases total blood pressure), but you are incorrect about the way that ADH gets released: there is no releasing hormone for ADH. Instead, ADH is released in response to one or more of the following:
1) Low blood volume (as in during a traumatic injury with a large amount of blood loss)
2) Low blood pressure (as detected by baroreceptors, aka pressure receptors, in blood vessels)
3) Angiotensin II (as part of the RAAS pathway, used in increasing BP)(12 votes)
- I'm confused about triggers and Na concentrations. Renin is released when the macula densa sense low Na levels but ADH is released when the blood is too salty? Is that because the low levels of salt the macula densa sense means a lot of salt had to be absorbed in the proximal tube and the loop of Henley in order to absorb more water? And this happens because there is a high osmolarity?(5 votes)
- ADH is released when osmolarity is high, too much Na+, because of dehydration. It causes retention of water by the kidneys, and it also causes vasoconstriction in the body to bring up blood pressure.
Aldosterone is released when Na+ is low and K+ is high. It causes the retention of Na+, and water follows the Na+ back into the blood while K+ is put in the filtrate. Both ADH and Aldosterone work on the DCT and collecting duct to retain water. They can work independently of each other.
Renin is released when blood pressure is low (and Na+ is low) in the nephron and it becomes Angiotensin II (2) It causes vasoconstriction and the co-release of both ADH and Aldosterone. All three work to increase blood volume and blood pressure to ensure normal GFR in the kidney. Yes, there is a lot going on. Basically, your body has several ways it responds to low blood pressure, BP, because without oxygen delivery our cells die. If the kidneys are not getting BP they are not getting oxygen AND the blood urea nitrogen, a waste product, is building up in the body.(8 votes)
- At, Rishi says that the body notices that the blood is too dilute. I was wondering how does our body know that our blood is too dilute? Do the Macula Densa cells tell the body? 7:42(4 votes)
- One way it could know is the arterial blood pressure, which Rishi describes in the case when ADH needs to be released in response to low blood pressure. When blood pressure is too high ADH is likely inhibited or an antagonistic hormone may be released to bring the body back to equilibrium.(3 votes)
- Whats the difference between ADH and ANH? Just asking cause i am totally new to these terms.(3 votes)
- ADH stands for Anti-Diuretic Hormone, whereas ANH stands for Atrial Natiruetic Hormone. ADH acts to increase water retention and increase blood pressure. ANH acts to decrease blood pressure. ANH, interestingly is a hormone released from the upper chambers (atria) of the heart.(4 votes)
- At the 5 min mark, Dr. Rishi indicated that ADH is carried to the rest of the body via the venus system as opposed to the arterial system? All other nutrients and oxygen are carried via the arterial system.
Is ADH carried to the rest of the body via the venous system?(2 votes)- It's carried to the rest of the body by the circulatory system, not just the venous portion of the circuit.(3 votes)
- At, Rishi mentions receptors in the large veins. What are the receptors in the large veins called? 11:28(2 votes)
- These receptors are still called Baroreceptors and they are mechanoreceptors that react to decreased vessel stretching (or lower volume/pressure). Blood volume, especially on the venous side, helps determine the blood pressure so you can still consider them to be Baroreceptors.(2 votes)
- At, Rishi says that the ADH hormone is 9 amino acids long, but it has the same affect on blood vessels (vaso constriction) as an 8 amino acid-long hormone, angiotensin 2. What is the difference between their effects on a blood vessel? could ADH do angiotensin 2's job if renin cut off 443 amino acids and ACE didn't touch it? 3:38(2 votes)
- They probably have different active sites and their "key" nay fit into a different lock which could cause a separate effect. Also, those AA's could be different or in a different order and one change in an AA could create a totally different protein than the previous one(2 votes)
- Do you mean milliosmoles instead of osmoles?(2 votes)
- Hi! Wouldn't salty blood (Increased osmolarity) mean that more water would move into the vessels, therefore increase blood pressure?(1 vote)
- That is correct! Aldosterone does exactly what you described. It increases the Na+ uptake from distal convoluted tubule and during the process, water follows. That means blood has more fluid than previously and will lead to higher blood pressure.(3 votes)
Video transcript
We're going to talk about
antidiuretic hormone. And you can see I've already
started drawing for this video. And the main reason is because
I'm not a great drawer, and I wanted to make sure that
everything was pretty clear. And so I drew out on one
side the pituitary gland and on the other the brain. And so antidiuretic
hormone-- I underlined ADH because that's usually
what it's called. People call it ADH. Sometimes people call
it vasopressin as well. Actually, vasopressin is
good because it's useful. You can see "vaso" kind of
refers to blood vessels, and "pressin" kind of squeezing
down on blood vessels. It gives you a clue as to
what the hormone is doing. So I've drawn for you
the hypothalamus here. Also, right below
it, this would be kind of the infundibulum,
kind of the neck. And at the very
bottom, the pituitary. So this is the actual
pituitary down here. And there's a front
and back to this. And the front, facing
forward closer to the eyes, would be the anterior pituitary. So that'd be over here. And back here, this lobe would
be the posterior pituitary because it's a little
bit further back. And since we're
naming stuff, let me just go ahead
and round it out. This right here is
actually the optic chiasm. It has to do with vision. So I'm just going to
write optic chiasm so you know what
we're talking about. And the only reason
I even bring that up is because just above it--
let's say in this area-- just above it. And if I was to draw it
over on my little diagram-- that'd be maybe right there--
is what's called the "supra"-- S-U-P-R-A-- supraoptic nucleus. And nucleus here just
refers to a collection of nerve cell bodies, not
the nucleus we usually think of-- meaning not the
one where it's sitting inside of a cell and kind of
directing the flow of traffic in the brains of the cell
in a way of saying it. But here the nucleus is
actually just a collection of little nerve cell bodies. And I'm actually just
going to draw two, but you know there's
actually many more there. This is just for
diagram purposes. And actually, if I was to
draw the rest of this nerve, you would actually
go all the way down. And this is actually beginning
to share with you some of the cool aspects of this
hypothalamus and the posterior pituitary. You can see that, basically,
these nerve cells start in one spot, and
they go all the way down to the posterior pituitary
through that infundibulum. This is how the hypothalamus
and posterior pituitary are connected-- through nerves. And these nerves are actually
full of the hormone ADH. So we've already
talked about the fact that this is related to ADH,
but now you can see exactly how. ADH is actually being
made in these nerve cells. And it's actually
sitting here waiting for the right moment for
these nerves to release it. And this ADH is actually
a small protein. It's nine amino acids long. So it's actually pretty small. This is ADH. Nine amino acids. So it's pretty teeny,
and it's a hormone. And if you know it's an
amino acid-based hormone, you can think of it as a
peptide or a protein hormone and distinguish it from
the steroid hormones. So this is how ADH is made. It's made in these nerve cells. And the next thing to talk
about is how it's released. And so if you have, let's
say, a little capillary bed in here with little
arterials and capillaries coming together into little
venules on this side, what happens is that, when
there's a trigger-- and actually, maybe
I should write that in a very bold color. Let's say red. That's my favorite bold color. When there's a trigger,
these nerve cells right here are going to fire off their ADH. They're going to
release all that ADH, and it's going to dump
right here into this area where all the capillaries are. And of course, the
flow of blood is going to carry all that
ADH into the little vein-- and let me draw the
venule and the vein-- and basically, take it
to the rest of the body. So this is how ADH
actually gets released out of the nerve cells that live
in the supraoptic nucleus and gets out to the body. It basically does it by dumping
into that posterior pituitary and getting picked up by
all those little capillaries and venules. So I guess the next issue is to
figure out what is the trigger? So what is the trigger for
this little supraoptic nucleus that I've drawn here? So let's talk about that. Let me make some space. There. Now, we've got a
clean bit of canvas. So let's talk about the
triggers that our body uses to know when to fire off
that ADH to get it released. The main trigger-- and this
is probably the one trigger that you want to take away. If you're going to
forget everything else, try to remember this one. The main trigger is going to
be high blood concentration. And the way we think about blood
concentration is in osmolarity. Let me write that down. What osmolarity refers to is,
if you took all the solutes that are floating around
in the blood-- so that includes everything
from protein to sodium to potassium, everything
that is going to drag water into the blood vessels--
if you combine all that, then what is your total blood
concentration going to be? And you can almost
think of it as a meter. So let me draw it for you. Like a little meter here. On one side, you've got--
let's say something like that. And on one side,
let's say you've got 260, and on
the other side 320. And this is just concentrations. So 280 and 300. And this is osms per liter. And actually, these
are the units here. So osmolarity as measured
in osms per liter. So this is the concentration. And what you want
to do is you want to really stay in
this area right here. This is kind of your green zone. This is where the body likes
to be, generally speaking. And if it's here, if
it's in this area, or if it's in this
area, then that's where the body is not too happy. And so for example, let's say
you're in this first zone. This would mean
that your body is noticing that the
blood is too dilute. And if it's on this
side, your body's noticing that it's too salty. The body is saying that
the blood is too salty. And so in this
case, if you have, let's say-- like I
said-- a meter down here, if the needle is
falling in this area, then that's going to be a
trigger for ADH release. So that's the first trigger
that we can talk about. In fact, why don't
I even go back up and add that to our diagram? So I'm going to put
that into our diagram so that we can see
it very clearly as being one of the triggers. So let's imagine you have
right here a little nerve cell. And I'm going to draw it this
way purposefully because we actually don't know where
these little osmoreceptors are. All we know is that
they do a fantastic job, but we don't know exactly
where these osmoreceptors are. And this is my little
diagram that I drew before. And you can now think, if the
osmoreceptor is telling you that it's over there,
then that's a problem. And in fact, why I don't
I even go one step further and label this as
my osmoreceptor? So if my osmoreceptor is set
to tell me that it's too salty, that is one of
the signals that's going to trigger ADH release. OK. So now, what's the
second trigger? What's another reason
why we might release ADH? Low blood volume. Think about that for a second. How in the world would
your body even know that the blood
volume is too low? Well, let's go back to basics. Let's go back to the heart. That's where I like to
begin because that's how I always think about it. Just very simply, what
is going into the heart, and what's coming out? Well, we know we have
blood vessels-- large ones, in fact, large veins--
dumping into the heart. So we have the superior
and inferior vena cava. This is the superior vena
cava-- this is a large vein-- and this is the
inferior vena cava. These aren't the
only large veins, but these are two
examples of large veins. And we also have
the right atrium. So we have a couple
of spots here that are in the
blood vessels where we might have little
nerve endings. So nerve endings
in these areas are going to start recognizing
when the blood volume is low. Because, remember,
the venous system-- this is kind of a stretch-- the
venous stretch from something we talked about a long time ago. The venous system
is actually going to be a large volume system. So if there's ever a
decrease in the volume, that would be one of the
best places to figure it out. So information in the walls-- so
basically, these nerve fibers, rather, in the
walls of the vessels are going to be less stretched. And they're going to say, well,
why are we less stretched? And the answer is that there's
actually less blood volume. So when they're less stretched,
they're going to send a signal and say, hey, something's up. We have less blood
volume, and I think the brain needs to
know about that. So that's how a signal gets sent
all the way up to the brain. And actually, I can
draw that in as well. So let's put in a
little receptor here. And now, these are going to
go down and sense low volume from those receptors
in the large veins and the right atrium. OK. Now, what's another trigger? You can see there are a
lot of different triggers. I'm putting up
one after another. Let's put another
trigger up there. What's another reason why
ADH would be secreted? Well, maybe a decrease
in blood pressure. Now, we know that
the veins tell us a lot of information
about volume. So it might extend that
the arteries can tell us about pressure. And you might recall
from another video where we talked about
baroreceptors that this is a fantastic way to get
information about pressure. So let me draw some of
those baroreceptors. And baroreceptor just
refers to pressure receptor. We have baroreceptors that are
in the aortic arch right there. And we also have
baroreceptors that are in the carotid
sinuses on both sides. So these baroreceptors are going
to recognize when the blood pressure is starting to go low. And they're going
to send a signal up to the brain to
say, hey, again, we need to do something about this. Our pressure is low. So that's another
signal up to the brain. And that we can
draw it right here. We could say, OK. Maybe something like this. And that would be a
signal about low-- let's write that
here-- low pressure. So now we've got signals about
high osmolarity, low volume, low pressure. Are there any other signals
that we can think of? One more jumps to my
mind-- angiotensin 2. Remember, angiotensin
2 is actually part of the whole RAS system--
the renin-angiotensin-- or I'll just write AT--
aldosterone system. And so angiotensin 2 is actually
going to be another trigger. So you can actually imagine
through a blood vessel, and you might have
a nerve nearby. And this is going to trigger
right here this molecule of angiotensin, which has
eight little amino acids. It's going to be a
signal to that nerve that it needs to let the body
know-- or the brain know, rather, that pressures are low. This is another signal. And let me just write that
up here in our picture. Another signal could
be something like this. Maybe right here. And the exact location
that I'm drawing is actually just
kind of arbitrary, but the idea is that
you have angiotensin 2 having effects on
the brain as well. So this little molecule
is going to come and let the brain know that, hey,
even the kidneys are trying to do something about
the blood pressure. And it would be great if
the brain got involved in releasing some
ADH, if needed. So these are the
different triggers. And like I said
in the beginning, probably the main one
you want to think about-- as far as ADH is concerned--
is this osmoreceptor. This is really the
most important one because everything else
is secondary to that. That is definitely the
major function of ADH.