Let’s take a look at the Posterior Pituitary.
At first, real posterior pituitary hormone here
Now, even though there are only two hormones
that we will be addressing here with posterior
pituitary, my goodness, the clinical applications
of these are massive, as you shall see.
First, what is this particular illustration
Understand where you are.
We’re in the collecting duct, we’re in
the kidney and we’re moving from our cortex
into the medulla and I want you to imagine
that beyond the collecting duct versus urine
osmolality of being 1200, beyond this, we’re
going into our minor/major calyces and then
out towards the pelvis and towards the-towards
Are we clear as to where we are now?
This is not the loop of Henle; we are in the
kidney and we are in the level of the collecting
duct and then here, with ADH, we’ll be referring
to its receptor being V2 receptors.
And with V2 receptors, remember we talked
about the vasopressin with V2 receptors and
its second messenger here will be Gs in fact…
not Gq, but Gs.
So, in the distal convoluted tubule that’s
responsible for increased water reabsorption,
thus with the help of ADH only in the collecting
duct can it move up to 1200.
Now, they can ask you a physio question here
by saying that without the effective ADH on
the nephron, where is it in the nephron that
your urine osmolality will be the highest?
It would have to be the loop, right?
Are you picturing?
And by that, I mean the descending loop of
Henle where you are reabsorbing your water,
but that has nothing to do with ADH, does
It’s only after you’ve understood that
point in which this sentence here where, with
the help of ADH and V2 receptors reabsorbing
water, you then form concentrated urine.
Next, a different location all together.
This is not-not the collecting duct, this
is not the nephron.
This is in reference to ADH and its effect
via V1 receptors on your blood vessels where
we are here.
Look at the arrows that you see here with
ADH and with the help of it, you’ll notice
that the blood vessel here on top is a lot
more narrow in calibre than it is at the bottom.
It kind of looks like a flask.
And the only reason that it looks like this
is because when a patient is dehydrated, when
releasing ADH, it is responsible for vasoconstriction
and this will be V1.
Along with this, understand that ADH will
then promote the release of von Willebrand
factor and factor VIII via endothelium.
Endothelium, of course, being the cells of
your blood vessel and you should remember
that von Willebrand factor and factor VIII
work together for optimum, optimum haemodynamic
So, vasopressin analogues for the management
of von Willebrand type 1 and hemophilia could
be used effectively, can’t it?
Amazing management vignette here, isn’t
It’s a fact that you may use an analogue
If you’re thinking about von Willebrand
disease type 1, understand that you’re deficient
of von Willebrand factor.
And if you’re deficient of van Willebrand
factor, you remember that patient who has
massive menorrhagia and the fact that you
have increase in bleeding time in PTT, why?
Because you need von-von Willebrand factor
for optimum functioning of factor VIII.
So, therefore, a vasopressin analogue could
in fact be used in this condition.
And then what about haemophilia A?
Haemophilia A is strictly deficiency of factor
Hence, you would only find an increase in
Here, once again, vasopressin could be used
to perhaps manage your patient with haemophilia
A by releasing factor VIII.
At supra-physiologic levels of ADH, it works
on V1 receptors to cause vasoconstriction.
It is important for you to understand that.
So, you need really high levels of ADH, so
you need to have a patient who is quite severely
dehydrated in which the influence of ADH on
your blood vessels would be taking place.
At low levels of ADH, as soon as our plasma
osmolality rises, let’s say above 300, then
your ADH will be released from the posterior
Just to keep things into perspective, ADH
is being synthesized where?
In the hypothalamus.