What about this RAAS system in aldosterone?
Let’s quickly go through the steps here.
Let’s say that you have a patient who has
decreased blood pressure.
Number one, if there’s decreased blood pressure
taking place, then as far as profusion is
concerned to the kidney in the afferent arteriole,
it is depressed.
The juxtaglomerular cells via your beta-1
receptors will be releasing rennin, ah, out
comes your renin.
The renin will then convert the angiotensinogen
which is coming from the liver... remember
ogen, ogen, ogen is a precursor.
Fibrinogen, angiotensinogen, trypsinogen,
pepsinogen, those are all ogens.
This is angiotensinogen coming from the liver
with the help of renin which behaves like
an enzyme, you have your angiotensin I.
Next, what happens?
What’s your… what is your objective here
and why would you even want to have angiotensin
II and why would you want to have aldosterone?
Because your blood pressure is decreased,
that is your inciting event, right?
Now, the first reflex usually is going to
be sympathetic tone, that’s a reflex that
The hormone, however, takes a little bit of
Also, the middle here that you see here, very
important physiologic concept of a really
quick feedback mechanism is called the MD
cells, the macula densa cells that you’ve
learned about in physio.
All of these amazingly will play a role so
that it-it restores blood pressure back towards
If it’s macula densa, it’s a reflex mechanism
and I’m just going to quickly tell you because
there’s decreased blood pressure, you have
decreased hydrostatic pressure over the glomeruli,
therefore decreased filtration, decreased
delivery of sodium to the macula densa cells
and therefore, what does it want to do with
the afferent arteriole to then increase the
GFR, the glomerular filtration rate?
It wants to vasodilate.
If you’re unfamiliar with that then please
refer back to physio and make sure that you
know what’s known as a tubuloglomerular
feedback… quite important, quite important.
In the meantime, let’s continue.
Angiotensin I with the help of ACE which stands
for angiotensin-converting enzyme is then
releasing angiotensin II and you tell me.
Our discussion here, angiotensin II stimulates
We have our aldosterone, what are we trying
Restore blood pressure back towards normal.
Hence, it will reabsorb sodium and water.
In the meantime, do not forget about a little
pharmacologic side effect, huh?
This is known as ACE inhibitors.
At any point in time, if you wish to give
an ACE inhibitor, which is normally responsible
for breaking down your bradykinin; if you
gave an ACE inhibitor, bradykinin will be
elevated, your patient is now complaining
of ugh, ugh, ugh… dry cough.
Angiotensin II, in addition, remember your
patient has decreased blood pressure; angiotensin
II overall is a potent, potent vasoconstrictor.
If you vasoconstrict an arteriole, you’re
increasing your TPR in the hope of increasing
A simple physiology question is the following.
If you inhibit angiotensin II, the vasoconstriction
has been lifted vascular and you drop your
after load increasing your cardiac output...
a simple physiology question in the formal
Down the kidney… afferent/efferent arteriole,
angiotensin II prefers to work-prefers to
work at normal levels at the efferent arteriole.
Remember, when you have decreased blood pressure,
what happened to profusion in the kidney?
Oh, it decreased, you have decreased filtration.
Wouldn’t you want to constrict the efferent
Think about that, are you there?
The efferent arteriole… if this is my-if
this is my glomerulus and this here is my
efferent arteriole, if you constrict this,
what then happens to your hydrostatic pressure?
Take a look at filtration fraction.
Remember this from physio… what’s filtration
fraction mean to you?
It’s GFR over RPF, right?
Please make sure you commit that to memory,
if you haven’t already.
It’s GFR over RPF.
If you constrict the efferent arteriole, what
happens to renal plasma flow?
Take your time… decreases.
Where is the RPF in the ratio?
In the denominator, so that’s decreased.
If you constrict the efferent, what happens
to hydrostatic pressure approximately?
What happens to GFR with efferent vasoconstriction?
Oh, it increases.
Now, this part, I can’t help you, this is
If you increase the numerator and decrease
the denominator, what happens to filtration
Obviously increases, there you have it.
Aldosterone works where?
Collecting duct, principal cells.
It works to do everything in its power to
On your boards, you can either work on the
sodium potassium pump on the basolateral membrane
or can work on the epithelial sodium channel
on the luminal membrane.
Either case, you’re reabsorbing sodium along
with that out comes the water in the hopes
of doing what?
Once again, increasing blood pressure.
Now, you’re reabsorbing sodium, keep it
Aldosterone wishes to get rid of two elements
into the urine.
It will get rid of potassium, it will get
rid of hydrogen.
Any condition in which there’s an increase
in aldosterone, you will then find hypokalaemia,
increased blood pressure and your pH is increased.
Because you’re getting rid of hydrogen…
Be careful, be able to do that quickly.
Create a favourable sodium gradient for sodium
and water reabsorption.
In addition, if you have decreased blood pressure,
that angiotensin II will do everything in
its power to restore blood pressure including
stimulating the posterior pituitary to release
ADH, as you know, will work upon your V2 receptors,
it will then open up the aquaporins, reabsorb
In addition, you increase your proximal convoluted
tubule… your proximal tubule… sodium reabsorption.
Once again, you’re trying to increase your
This is what something that’s called can
permit contraction alkalosis.
What that means is the following.
Water reabsorption can permit contraction
alkalosis, meaning to say that you would have
increased proximal tubule sodium reabsorption,
you get rid of your hydrogen and may result
in contraction alkalosis.
Stimulates the hypothalamus for thirst, once
again all… you begin with your inciting
event being decreased blood pressure.
Be able to go through this in great detail
and you should be able to answer any angle
of patho-physiology that they might ask you.
Angiotensin II affects baroreceptor function,
limit reflex bradycardia.
ANP, atrial natriuretic peptide.
What does it do?
Well, if it works in the atrial in response
to increase in volume, it will do everything
in its power so that it checks the amount
renin-angiotensin aldosterone, so check and
balance, check and balance.
If there’s too much fluid retention, ANP
will be released… atrial natriuretic peptide.
Later on, well, in cardiovascular, we’ve
talked about a very important marker known
as BNP and that becomes important too in a
patient with congestive heart failure.
This is ANP, atrial natriuretic peptide and
it will then increase your GFR.
If anything, it will cause vasodilation, relaxes
vascular muscle via cyclic GMP.
ADH also will regulate volume and if there’s
decreased blood pressure and if it’s significant
enough, not only will you have your aldosterone
but you’ll also have ADH and this would
then reabsorb your water.
Aldosterone, we’ve talked about in great
Low blood volume is prioritized at all costs.
That’s an important point.
I expect you to know from physio that if you’re
losing enough blood… so, you have a patient
that gets into an accident or gets into a
knife fight, huh, and gets lacerated so badly
that they’re losing massive amount of blood,
there it is on the floor and it keeps leaking,
At that point, what becomes more important,
osmolality or volume?
So, the body will do everything in its power,
This is hypovolemic shock.
Everything in its power to make sure that
it’s restoring the volume, restoring the
blood pressure, otherwise your patient’s
Hence, you have these hormones such as aldosterone
and ADH that will play a major role.