please. That is an important point
You go into further detail here , make sure
we set all this up. This is specific with
the principal cell of the collecting duct
and effect of aldosterone. Once again we have
the blood at the bottom, which means the basolateral
membrane aldosterone may stimulate that.
On the luminal membrane, you will notice a sodium
channel. The urine you see would be the lumen.
So reabsorption will be which way please?
Top to bottom or bottom to top. I am just
giving it every perspective. Reabsorption
would be from top to bottom, correct. Next,
there is the intercalated cell. So what kind
of substances might you be thinking about
here? Hydrogen. You pay attention to hydrogen
in this picture. Intercalated. How do you
form hydrogen now? The reason I love this
picture is because why I assume that you knew
that hydrogen and bicarb always are going
to run through that formula. You are seeing
that over and over again right. Now, what
is also important here? Bicarb produced.
So differences to the following. If you are not
following what I am saying, it's okay. Listen.
In the proximal convoluted tubule, go way
back proximal. In the proximal convoluted
tubule, tell me please about that bicarb.
Was it newly synthetized or was majority of
it was reabsorbed? Majority of it was reabsorbed.
80%. Here if its bicarb that is required
in the distal convoluted tubule, then understand
this is newly synthesized bicarb. Now ultimately
with aldosterone, hydrogen is then going to
be pushed out and bicarb is then going to
be reabsorbed inducing metabolic alkalosis.
Aldosterone, lets talk about spironolactone.
This is one in which we call this as being a
aldosterone receptor antagonist in the situation
in which if your blocker affects of aldosterone,
what are you going to do? You are not going
to get rid of potassium. You are going to
spare it. You are not going to get rid of
your hydrogen. You are going to keep it and
may result in decreased pH. What about ACE?
ACE inhibitors inhibit angiotensin converting
enzyme and never form angiotensin II. Stop
there. That angiotensin II which is a huge
vasoconstrictor, which would if present and
causes arterial vasoconstriction would contribute
to what? Afterload. If you give an ACE inhibitor,
you remove angiotensin II, listen, then you relieve
the arterial vasoconstriction resulting in
decreased afterload, point number 1. Point number 2, ACE
inhibitor, when would you even think about
giving ACE inhibitor? What about that patient
in which you want to decrease mortality? After
having a congestive heart failure event. It's a
good drug, isn't it? Because it decreases afterload
by inhibiting angiotensin II? How does it
decrease preload more so? Well, what about
aldosterone? If you can't form the angiotensin
II how in the world you are going to produce
your aldosterone from the glomerulus of the
adrenal cortex. You cannot right. So if you
don't have aldosterone, tell me about preload.
It is decreased. Important treatment for what?
CHF. Because it decreases preload, it decreases
the afterload. It's great because it decreases
angiotensin II subsequently aldosterone. We
have talked about angiotensin II and its effect
on arterial vasoconstriction. Here we go. We remove
the angiotensin II to decrease the afterload.
Aldosterone if present increases preload,
if inhibited, what do you do? You inhibit