The Renin-Angiotensin-Aldosterone System (RAAS) is a critical hormonal cascade initiated by the kidneys to regulate blood pressure and fluid balance, serving both daily needs and emergency responses like dehydration or bleeding.
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So if you can understand that then you
can understand the renin angotensin
eldoststerone mechanism
and let's just overview that mechanism
right now. The first thing that you need
to do to understand the reninangotensin
aldoststerone mechanism is to understand
that it orchestrates just about
everything, every hormone and just about
every mechanism that we have so that we
can increase the blood pressure. So just
by secretreting one thing the kidneys
can set off this cascade of events
that's going to be very valuable in
increasing the blood pressure.
Another thing that you need to do to
understand the reninotensin
eldoststerone mechanism is to understand
that we can use it in two different
ways. Basically one way is just in the
normal course of every day. You know, we
need it every day to a certain extent.
Adjusting the blood pressure, adjusting
the fluid volume,
it's our main mechanism for those adjustments.
adjustments.
But the other way is that we can use it
as a panic button, basically as a way to
really fight against things like
dehydration and bleeding to death. You
know, when we just simply have too
little volume to survive, we're going to
hit that panic button. And when we're
doing that, we're overusing the renin.
We're really oversereting the renin,
overusing that cascade.
And basically what I want you to do is
think of, you know, a lot of our chronic diseases
diseases using
using
the stress hormones
to that acute
panic button stage rather than just the
normal everyday living type of stage.
And as still as an overview, what does
it do? What does the cascade do in the
very end as it changes to the ultimate
what we call stress hormone angotensin
2 that's a stress hormone that's one of
our most potent stress hormones you know
I can name just a few others like
cortisol that are as potent or more
potent so angotensin 2 is a potent
stress hormone and one of the things it
first does is constricts the blood
vessels. So, straight away it's going to
be increasing that peripheral
resistance, isn't it? Constricting those
blood vessels, increasing the peripheral resistance.
resistance.
The another thing that it's going to do
is go up to the posterior pituitary
gland and and be the primary reason for
the release of ADH, the water saver.
That's a a very potent mechanism. You
combine it with blood vessel
constriction with something that affects
the eldoststerone and something that
affects more adrenaline, you've got a
really potent uh combination of things
that a really potent uh cascade of
events. So another thing that angotensin
2 does is it releases eldoststerone the
salt saver. So along with salt being
saved the water water is saved and that
increases the volume of blood and
finally it inhes more adrenaline and
then the other thing that I wanted to
say just as an overview about this
angotensin 2 it's just go back to the
fact that I said that chronic disease
almost always results in fibrosis and
scarring anytime time you have a chronic disease,
disease,
a patient with a chronic disease, what
our job is to do is to try to make sure
that that resolves that that we resolve
that before this this stuff happens,
this other stuff, this chronic disease
always results in fibrosis. And in this
instance, what is making the fibrosis is
this guy right here, angotensin 2. It
goes over to it not only does this, but
I'll I'll show you some other things as
well, but it goes over to the heart wall
in the ventricles. It actually results
in what they call a remodeling of the
ventricle. And I mean, you know, the
heart is perfect just the way it is. You
start messing with it and putting
fibrosis and scarring and remodeling it,
it's not it's not going to have that
that that good flexibility. it's not
going to have the the qualities that it
needs to be of optimal benefit to us.
The blood vessels, it remodels the blood
vessels. It actually angotensin 2 has
been found to increase the amount of uh
atheroscllerotic developments. It's uh
been found to harden the arteries in
itself and through the process of atherosclerosis
atherosclerosis
and also uh we we can uh kind of relate
that to something that happens at the
kidneys too because there's a thing
called diabetic glomeular
glomeular
sclerosis. That word again, sclerosis,
hardening. Hardening. What is hardening?
When when we hear hardening, we're
thinking, yeah, it's probably scarring
it. So gl diabetic glomeular sclerosis
is it's you you'll just know it in the
future as u as just diabetic uh kidney
disease. You probably noticed that. So
it's something that stops the angotensin
2 from developing will be good in all of
those areas in the heart wall in the
blood vessels and in the kidneys.
So what we have been talking about so
far with respect to the renin angotensin
aldoststerone mechanism
is mostly having to do with angotensin
2. Angotensin 2 is that called that
potent stress hormone and it has all of
those direct actions.
Now what we're going to do is take a
look at this flowchart. You've probably
seen this flowchart before. It's a
really good flowchart with respect to
the renin angotensin aldoststerone mechanism.
mechanism.
In order to understand this flowchart,
you kind of have to understand where angiotensinogen
angiotensinogen
comes from. This one right here. Angotensinogen
Angotensinogen
is an inactive
hormone. It's a it's really a precursor
of angotensin 2. And what we do with angotensinogen
angotensinogen
is we excrete it from the liver just to
kind of be around and to be ready for a
situation in which it's needed. So we do
that a lot of times. We do that with you
know the coagulation proteins
and for instance in the coagulation
cascade we'll have one protein set off
another and another another and we get a
lot of benefits from that because
they're always kind of hanging around
always there ready to do something at
that point they're not really doing
anything but they're ready to do
something. So we've got angotensinogen
always floating around ready to do
something and then we've got the
stimulus at the level of the kidneys.
And remember those stimuli are the
decrease in pressure at the kidney or
sympathetic nervous system stimulation
to the afrant arterial.
And when we stimulate the release of the
renin that goes out into the system, it
changes the angotensinogen to angotensin
one that's still inactive though. We've
got one last step and that step is going
to rely on an enzyme. The enzyme we're
talking about is ACE angotensin
converting enzyme. So we convert
angotensin one to angotensin 2 and with
that conversion we've converted it to
the active and potent stress hormone
angotensin 2.
So where do our drugs work? We've got
two major drugs in this cascade of
events. We also have a drug that we
seldom use. It's called a direct renin
inhibitor. It's called Alice Skyin and
it's got too many adverse effects to be
a valuable pharmacological treatment.
So, you should probably know that we do
have some direct
renin inhibitors, but we don't really
use them very often.
The other two, the two that are really
often times used are the ACE inhibitors
and they work right here inhibiting that enzyme
enzyme
and also the angotensin
2 receptor blocker. Remember back when
we were talking about the broad ways in
which we have our drugs work. The one
way was inhibiting an enzyme and we're
doing it right here. We're inhibiting
the ACE, the ACE inhibitors. And the
other broad way in which our medicines
work is by binding to a receptor. And
that's where this one works. The the
angotensin 2 receptor blocker. And that
brings us to the first of three subsets
of questions in this tutorial. You will
need to take this question down now as
it's not going to be available on the
PowerPoint slides and it's not going to
be available anywhere else. So the
question goes briefly explain the renin
angotensin eldoststerone mechanism
placing the prill and the sartin drugs
into the context of that explanation.
include a list of organs identified in
the tutorial that angotensin 2 acts on.
We have just gone through that but just
as an overview so that you can
understand the question and start to
answer it. Remember to use this
flowchart while you're developing your
answer because it's a really good
flowchart and it's also going to help
you develop a accurate answer. Also
remember that candaceartin the sartin
drug is an angotensin 2 receptor blocker
and as such it blocks the receptors that
we have in this list here.
But aside from that it also blocks the
receptors in the heart and the kidneys
as well as you'll see in this diagram
right here.
So, right now, I'd like you to start
developing your answer. We just went
through this. So, if you do a really
rough draft while it's fresh in your
mind, it'll be most productive.
I'll pause the recording, and that means
that the students who are working off of
the video tutorial series are going to
Okay, so hopefully you've started
jotting things down on how you're going
to answer this portion of the question.
It's worth just three points, so it's
the easiest portion of the multi-part
tutorial question, and you should be
able to do it in about 125 words or so.
In that way, you're going to leave the
majority of words for the two questions
that are weighted much more heavily.
Remember that the question goes briefly
explain the reninangotensin
aldoststerone mechanism. Placing the
prill and the certain drugs into the
context of that explanation include a
list of organs identified in the
tutorial that angotensin 2 acts on. So
the very first thing that I'd say to
start out with would be a bit of an
overview of the renin angotensinostrone
mechanism. So I'd say something like the
renin angiotensinostone
mechanism is a hormone system that
regulates blood pressure as well as
fluid and electrolyte balance. It's our
way of increasing the blood pressure
using every mechanism that we have
simply by releasing renin from the kidneys.
kidneys.
So that gives the reader a good overview
of why it exists and what it is. And
then you would probably start at the
beginning of this flowchart and go
through the steps of the renin
angotensin eldoststerone system. So
renin is released from the kidneys in
response to the sympathetic nervous
system stimulation or by a detection of
a lower blood pressure at the level of
the kidneys. And then renin changes an
inactive circulating hormone called angotensinogen
angotensinogen
to angotensin 1. Angotensin one is then
uh converted to angotensin 2 by an
enzyme mostly in the liver uh but it's
elsewhere as well. So but you can just
say in the liver and that's called ACE
angotensin converting enzyme. So once
again you say angotensin converting
enzyme you put it in parentheses acce
and then from that portion from that
point on you can keep using the ACE abbreviation
abbreviation
and that's where our ACE inhibitors work
preventing the angotensin one to form
angotensin 2
and then the angotensin 2 acts on organs
including ing. And then you would look
through each one of these organs listed
here. The adrenal medela, the renal
tubules, the adrenal cortex. Not just
the adrenal gland, the adrenal medela
and the adrenal cortex,
the uh arterials and the posterior
pituitary gland. So not just pituitary
gland, the posterior pituitary gland.
And there's also receptors in the heart
and the kidneys.
And of course, that all has to be in
your words, not in my words and not off
the website. But just to explain it a
little bit more for this subset of the
question, you only have to list the
organs that I just mentioned that have
the angotensin 2 receptors at this
point. But in the next question, you're
going to need to know what happens when
angotensin 2 receptor blockers block
each one of those receptors. So let's go
through that really quickly. At the
level of the adrenal medala, remember
that the adrenal gland has the two
portions. the medala which is the
sympathetic nervous system the middle
portion of the adrenal gland the
sympathetic nervous system and the
adrenal cortex which is the outside
portion and that secretes steroidal
hormones like eldoststerone the salt
saver. So at the level of the renal
medela, angotensin 2 increases the
sympathetic nervous system release of noradrenaline
