Concentración y Dilución de Orina

Welcome to this new class

on renal physiology. Last class

we talked more about

urine information, all about

filtration, resolution, and secretion of

urine. In this class, we're going to talk more

about concentration and secretion, that is, we're going

to focus a little more on

the renal medulla. Yes, of course,

this class will also

have a discussion next Monday,

where we can exchange anything that

wasn't clear. If

more students with questions,

not only about the theoretical class but

also about the practicals, are welcome to come and

interact. This is another way for us to have

a closer

exchange of ideas so that the

knowledge is more easily understood. So,

let's begin with

today's class, which is about urine concentration and

secretion.

What can the kidneys of mammals do? It might be

a little confusing, but I'm going to give you some

examples of what happens in our

bodies because it's the same thing that happens

in domestic animals

and mammals as well.

So, I'll try to give you

some examples of... What you see

in your bodies,

what you notice, is

also applicable to patients.

First of all, the kidney can change

the composition of urine depending on the

body's need to eliminate

one substance or another. What does this mean? It means that

our kidneys have the ability

to

concentrate urine, that is, to increase the

amount of water and reduce the concentration. This occurs

when our

internal environment or our blood is in a

state of hyperosmolarity.

The opposite happens if there is one or

two solutes in our blood; it is diluted, and

our internal environment will also

be diluted. In this case,

our kidneys have to

eliminate the excess water and retain as many

solutes as

possible.

In this class, we will learn about the

mechanisms by which the

kidneys can eliminate excess

water, creating both dilute urine and

conserving water by excreting concentrated urine. We will also learn about

the nervous and hormonal mechanisms

that control the osmolarity of

body fluids by adjusting

the kidneys' ability to concentrate or dilute them. We already covered this in

the last class, but we will

review it because that's what we'll be

discussing.

You remember, of course, that the kidney

has a cortex and a medulla. Yes,

where we're going to focus more attention are

these types of neurons, the

medullary neurons. Yes, those you

remember from the last class, they had

long loop shapes, they almost reached the

renal papilla, and they have the

peculiarity of being

accompanied by a prolongation

of the peritubular capillaries

called vasa recta. They

are straight and will be

important for the process of

concentrating and diluting urine.

What I'm showing you here is an

enlargement of what's in the medullary apparatus.

Why? Because we're also going to

consider in this area what's missing. What's

missing is a structure that affects

the medullary apparatus,

specifically the artery, the glomerulus, the artery

different from the capillary filaments, the

filtration membrane in the urinary pole. And what

we're missing here is the

glomerular apparatus, which we'll go into

more detail about. We'll try to keep

this lecture from getting too long. Not a 45, but rather

a bit more limited. In any case, we'll

address the questions raised in

Monday's talk.

We'll reiterate that when

plasma's popularity is low,

our system resorts

to feedback and

nervous and hormonal mechanisms.

This way, the kidneys

eliminate excess water through urine, resulting in

dilute urine and promoting

water elimination from the body.

What happens when osmolarity—you might

find it written as "osmolarity"—is high (it's not misspelled as "

molality"), but it's actually "

osmolarity" (it's a

calculation error). It's a

molar ratio, and you'll

find it written either

way. What happens when molarity, or

polarity, is

high,

meaning our internal environment has a

lot of solute and little water? Then,

nervous and hormonal feedback systems are activated again.

The kidneys excrete excess solutes,

decreasing water loss. This results in the

excretion of concentrated urine,

as I... I can tell if there's

concentrated or dilute urine by the

color of the urine, and we also do

urine analysis, including density—all the

physical and chemical aspects

of urine analysis that you

saw

in the practical part of the last class.

Here, what we're looking at is a

diagram taken from a deluxe

veterinary physiology textbook. What we see here is the

kidney size of different

species,

the percentage of long-loop neurons

in those species, the relative thickness of

the medulla, and the maximum

freezing point depression of the urine. What

I can see in this diagram—

look at the dog, for example—the dog

has a kidney size of 40 millimeters,

the cat has 24, that is, practically

half. The human has a much larger kidney,

64 millimeters. But notice the

detail that interests us most: the

percentage of long-loop neurons. The

human has 14%. What does this mean?

Because we'll see that the

concentration of urine depends on these

long-loop neurons, and of

course, on the thickness of the medulla. The

thicker the medulla, the more it means that... The

longer these neurons are, the longer the loops

of these neurons. Therefore, we'll

see that it will have a greater capacity

to concentrate. What we

see here is the abysmal difference

between a dog that has 100%

long loop areas and a human

who has 14% of those long loop areas.

Then there's the kangaroo, which is more

or less at the same figure, and

after this, the samurai. No desert rat

has 100% of those long neurons in

a kidney that is 13 millimeters in diameter. And

look at the thickness of the medulla; even the

medulla is at 10.7 points. I said

the set of other specific neurons is, for

example, that of the human, 3%. The beaver, because it

has, look, a

relatively large kidney, 36 long loop neurons,

0%, and the relative thickness of the

medulla is 13. That is, it has a lot of cortex and

little medulla. The beaver, for example, is an

animal that lives in a

practically aquatic environment. All

aquatic animals will not have the

need to concentrate urine because they

live in the water, so they

basically don't need to

concentrate the urine; they only have to...

Eliminating waste, on the other hand, animals,

or in our case, those of us who don't live in an

aquatic environment, have to be able to

concentrate our urine in the face of greater

scarcity, or in the case of going

many hours without drinking water.

This little desert animal obtains water

not only by concentrating its urine and

avoiding water loss, but also

through the metabolic water

produced by the water it consumes along with its

food. Because what is the

difference, for example, with a dog or a

cat? While the dog consumes much more

water than the cat, its

data shows that a poor water drinker is

always... Walter

has those habits, that is, it has certain ways of

drinking water, or it doesn't drink water

from just anywhere in its bowl, but rather from places it

goes. The kitchen

has its own way of doing things. On the other hand, if you

put a bowl of water in front of a dog, it will

drink water from anywhere.

The animal in that case is the same as what happens

to us when we have a lack of

water or an absolute excess in our

body. What we do is trigger

the thirst reflex,

so that individual looks for water and

tries to drink it in one way or another.

So that is what

this diagram shows us: the percentage Let's talk about the

importance in animals

that don't live in aquatic environments. The

percentage, the number of

those long neurons, will be able to

more efficiently prevent water loss.

Next, let's talk about

which hormones are involved

and which will help with this

urine concentration. We'll have

several hormones in all our

processes, in the

functioning of all our

organs. Hormones will act. We'll just

look at what's normal in other

classes when we specifically look at

hormones,

the definition of all hormones. If

possible, we'll name some, not all,

and see where they come from and

what function they perform. But in this case,

the main hormones in this

process,

one of them, will be the

hormone aldosterone. In this state,

what aldosterone does is increase the

reabsorption of sodium and cause

the excretion of potassium. Actually, what the

stimulus is for

the release of this hormone is excess

potassium. More than retaining sodium,

retaining sodium is a secondary effect; it's mainly about being able to

eliminate potassium from the body, thus preventing

hyperkalemia. Hyperkalemia is an

excess of potassium, hypokalemia. It's the

potassium level, with a decrease below

its physiological limits.

Hypernatremia is an excess of sodium, and

hyponatremia is a lack of sodium, a

decrease below its

normal physiological limits.

Where does this hormone, aldosterone, come from? Well, this

hormone, aldosterone, comes from

the adrenal gland. Yes,

you remember that we had an

adrenal gland that

also had a cortex and a medulla. The

adrenal medulla produced adrenaline,

noradrenaline, and catecholamines, and the

adrenal cortex produced mineralocorticoids

and corticoid groups.

Within these mineralocorticoids

is this hormone, which is aldosterone.

Yes, because it's called mineralocorticoids

precisely because it acts on the

elimination or retention of

certain minerals.

Of course, it will also help in

everything related to the concentration or

elimination of water, and modify the

characteristics of the urine.

What does this hormone respond to? As you can see

behind this extreme,

the bull needs it from adrenocorticotropic hormone (ACTH),

and you're seeing

corticotropin. Where does it come from? From the

pituitary gland. Remember that in the

central nervous system we have the hypothalamus,

which is closely connected to the

pituitary gland. The pituitary gland had an

anterior part (there are other classes coming up),

but to remember a little bit so you understand

hormones,

the pituitary gland had an anterior part (

the pituitary) and a posterior part (the

pituitary). In this case, we're going to

consider both parts of the

pituitary gland because the

pituitary gland will produce adrenocorticotropic hormone (ACTH).

If it's released,

ACTH travels via the bloodstream to

the adrenal cortex, stimulating the

production of aldosterone. And that ACTH will have an

effect on the

collecting ducts to retain

potassium and eliminate it through urine.

But another stimulus that also produces

the release of aldosterone is when we

have angiotensin II circulating in the blood.

This comes

indirectly from the glomerular apparatus.

This angiotensin II

is also a direct stimulus for the

production of aldosterone. As you can see,

in this The hypothalamus

is closely connected to the pituitary gland,

also called the hypophysis.

Adrenocorticotropic hormone (ACTH) is released

from the pituitary gland, which then releases it from the adrenal gland. The

adrenal gland produces

aldosterone.

These hormones enter the bloodstream and travel to where they are needed. This is how their

function works. When there is an increase

in potassium intake,

the plasma potassium concentration increases.

This increase in

plasma potassium concentration triggers

all of this. Because if we

have an increase in

plasma potassium concentration, this

information travels through the bloodstream

to the central nervous system and

the hypothalamus. This

triggers the release of

releasing factors that stimulate the release of

ACTH, and so on, as we saw in

the previous image. As a

result of all this,

two hormones are released: aldosterone acts on the

cortical collecting tubules,

causing potassium to be released, meaning

the excess is eliminated. Potassium, of

course, retains sodium secondarily,

and this leads to the expression of potassium, and

we return to our normal

plasma potassium levels.

So, we're going to look at several images

here.

Aldosterone, then, the

variable absorption of sodium in the digital tubules and

the cortical collecting tubules. That's why it

eliminates potassium but reabsorbs sodium.

If you do sodium and potassium exchange,

then at the level of this Monday, which is

telling me less about the part with this, would

be the thick, thin, convoluted, proximal,

thin, or hairpin loop,

the thick ascending limb, the

convoluted tubule, crystals, and the

collecting tubules and connecting tubules. They will

always have a cortical part,

as you see in all systems, and a

medullary part.

So, in that way, to eliminate potassium,

the tubular cell eliminates potassium and salt

into the lumen of the tubule and brings sodium

into the cell and thus

into the internal environment.

Therefore, potassium is lost in

urine.

Factors that will stimulate the

production of potassium, but not of the

adrenal gland and the adrenal cortex,

the increase in the

circulating concentration of action intended, as we

had previously said, this Let's

see where sancio tensin 2 comes from, but

something is bleeding, seen in the

blood pressure section, and when they gave

blood pressure because one of the ways to

talk about blood pressure in the long term

is the renal system,

the increase in

potassium concentration in the extracellular fluid

and the decrease in

sodium concentration. This is secondary; the

important climate to which it will respond most is

the excess of potassium rather than the lack

of sodium, but this also stimulates

its release a little.

What happens if the extracellular volume

decreases? When we talk about the

extracellular volume, we're talking about this

fluid volume, or in this case,

basically the blood.

When the extracellular volume decreases,

meaning there's a lack of fluid,

blood pressure drops. Of

course, if we lose fluid, the pressure goes

down; they gave you that in the

blood pressure class.

This will cause an increase in the activity

of the sympathetic nervous system; that will

also add to blood pressure.

One of the ways to regulate

blood pressure is the release of

catecholamines. Yes,

this will basically

decrease it; we already saw that in the

previous lecture. When there is a release of

adrenaline and noradrenaline, it produces

vasoconstriction, and above all... The

afferent arterioles of the vas deferens

decrease blood flow to

the kidney, and in this way, the release of

angiotensin is released. We'll

explain the complex mental state later,

but basically, I'll tell you quickly,

remember that the

system isn't in the medulla; the

arterioles that transform

angiotensinogen, which circulates in an inactive form,

have to pass through the

point of being transformed into angiotensin II,

and there it has a vasoconstrictor effect. Yes, that's why

this is one of the ways

angiotensin II directly stimulates

the adrenal cortex for the

release and prior production of

aldosterone. Remember that aldosterone

is

a corticosteroid.

Another hormonal participant that

will also be very

important is the antidiuretic hormone,

abbreviated as ACTH, and also

called vasopressin.

This antidiuretic hormone or vasopressin

is the main signal that determines the

formation of a Concentrated or dilute urine,

where will this

antidiuretic hormone or vasopressin come from? Here we have

the axis. Half of it will also come from the pituitary gland,

but from the neurohypophysis.

If

it's antibiotic,

but where is it produced? It will be produced

in the neurons of the

supraoptic and paraventricular nuclei of the

hypothalamus. That

is, neurons in

the hypothalamus produce it, and with a

transport protein called neurotransmitter, it

sends it to the

posterior lobe or neurohypophysis, and there it is

stored until its use is needed.

When its use is needed, it is

released from the neurohypophysis. It travels

via the bloodstream to the

collecting tubules to retain water.

This hormone will open channels that

will cause water to pass from the

collecting tubules into the

interstitium and from there into the bloodstream.

In this way, the urine, in

a reduction of flow, will be

concentrated. You know we're going to talk a

lot about antibiotics. Vasopressin, and

what is the stimulus for its production

in the hypothalamus? In the hypothalamus,

we have nerve cells,

of course, called

receptor cells.

What happens if the blood

arriving

at the nervous system has a

hyperosmolarity, meaning it is concentrated?

These cells contract and

send a signal, and

the cells of the nucleus begin to produce the

antidiuretic hormone (ADH). Yes, the stimulus is

also seen to develop, or rather, to

activate the mechanism.

That is the most important stimulus for

the production of ADH. What type,

quantity, and

concentration of the blood arriving at the

nervous system,

and what situations

increase the release of

ADH? As we already mentioned,

plasma concentration is one of the most

important factors because it determines how the

blood reaches the brain.

It is the quality of the blood that arrives when

the blood volume decreases, that is,

when there is a loss of blood, whether

due to

bleeding through an ulcer,

for example, or it could be an accident

that is causing a A fracture

that is causing a loss of some

important step, but what happens in these

cases so that there is an increase in

antidiuretic hormone due to a decrease in blood volume

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the mouse can hear the noise

so that it increases due to an increase in plasma volume.

Plasma volume has to

vary very little, if in values ​​of

1-2%, its levels. On the

other hand, for

antidiuretic hormone to be released due to a decrease in

blood volume, the decrease in blood volume

has to be more than 10% so that it

has the stimulus of the previous etiology

to be produced and released. Yes, that is to say, it is

much more efficient for the

release of antidiuretic hormone a modification

of the plasma modality than the

decrease in blood volume or loss of

blood rate or loss of many fluids

due to massive dehydration. Let's suppose

that.

Basically, what will be most

released in antidiuretic hormone is with the

values ​​of the plasma volume

when blood pressure decreases, and

when blood pressure decreases,

why will it be released? We already said that the

kidney is the organ that regulates

blood pressure in the long term, therefore, the

antidiuretic hormone that ends

releasing has a direct way the

adrenal cortex for production

[M [Music]

Sorry, it will

also directly stimulate

the hypothalamus, which we will see in

a diagram for the production of

antidiuretic hormone, since the

adrenal cortex, which I mentioned again when I said "

perón," in this case, the decrease in

blood pressure will

generate the production of elliotamine

2, which also stimulates the

nervous system for the production of antidiuretic hormone.

But it has to do with angiotensin and

with the responses that the kidney generates

to a decrease in blood pressure.

Nausea also

generates, to a lesser extent, an

antibiotic release. Hypoxia,

the lack of

oxygen in the blood

and tissues, also causes some drugs like

morphine, nicotine, and cyclophosphamide.

Morphine and cyclophosphamide are

drugs widely used in veterinary medicine as well as

human medicine.

These increase

antidiuretic hormone production, and what

reduces antidiuretic hormone release?

Vasopressin, the decrease in vasopressin, if the

increase increases the release of the

diuretic, the decrease in vasopressin and the

production of antidiuretic hormone.

The increase in blood volume is the

increase in the Bohemia, the increase in

blood pressure, that

is, what happens when I

have high blood pressure?

The antidiuretic hormone's

production and release are blocked,

therefore there is no

water retention because if

blood pressure doesn't increase, what I have to do

is

eliminate some water to lower

the pressure inside those arteries. That

is, there doesn't have to be a

very marked vasodilation; there has to be

a loss of fluid for

blood pressure to decrease.

The drugs that produce and

reduce the release of antidiuretic hormone include

alcohol, clonidine, which is an

antihypertensive, and haloperidol, which is

a dopamine blocker. Haloperidol

is used in

veterinary medicine, and in this case, I'm

going to give you an example of what happens in

our bodies with alcohol.

Let's take a moment to consider

that you may have noticed that when you

drink alcohol, whether it's beer or

wine,

what happens is that

you produce more urine,

yes, but you're not drinking enough

fluid. So what does this mean? That if I drink, let's say,

a bottle of beer, I'm

going to eliminate more than a A liter

of urine, yes, why? Because what alcohol does

is

inhibit the action of the antidiuretic hormone.

So what happens is that

our kidneys don't have the capacity to

concentrate the urine properly,

so a greater amount of fluid is eliminated

than what is consumed. That's why,

after

drinking a lot of alcohol, younger people

are calmer, but on those days of

partying and such, the next day one feels the

need to drink water, water, water,

because, in reality, they are dehydrated. So, they have to

compensate for that fluid loss by

drinking water.

That's the effect of

alcohol. Basically, what alcohol does is

make one lose a greater volume of

fluid because it affects

this hormone. It inhibits the action of the

diuretic hormone, therefore

a fairly high percentage of

the kidneys' capacity to concentrate

urine is lost. So that's

also why,

when one drinks alcohol, one

urinates more than normal.

How does the antidiuretic hormone work?

The antidiuretic hormone, well, we had said

that it is released from the neurohypophysis or

posterior pituitary gland, it goes to have an

effect and acts on the distal

and collecting tubules. More or less in the

same places where the 20 nahs have an effect,

what

this tubular cell and collecting duct does is—it could

be a distal cell of the

distal convoluted tubule or the collecting duct, it

could also be the

internal cortical or medullary collecting duct—into

the cell, and from the

cell, of course, into the internal environment, into

the circulation, the water, and therefore it

decreases diuresis if

urine with concentrated characteristics is eliminated

because I suppose here in this place I mentioned

aquaporins because they are exclusive to

water.

If you are familiar with the old book, what you

will find is that the

mechanism of action was not known. Now it is

known. In the newer books, you

will find

these descriptions; look at them when you have time.

But I will summarize for you that

what we have in the

cortical and collecting tubules are three

different types of aquaporins. They are

proteins found in the

cell membrane.

There are aquaporins in different parts of the

body, choline

in the cells of the epidermis, and coenzyme in the glands,

the cilia that serve for

sweating and for fluid loss.

There are aquaporins. In practically all

the cells of our

body, in this case we're going to

talk specifically about aquaporin-

2, which is what this antidiuretic does.

Basically, what these proteins do is that they

are normally internalized.

When the aquaporin reaches the

vital convoluted tubules and

collecting ducts, it forms

channels through which water

passes directly. Once

the function of that antidiuretic is finished, these

proteins are re-internalized,

therefore they stop forming that channel through

which water flowed freely.

Basically, here I explain the entire

molecular mechanism of how

aquaporins work. I

explained it in a slightly more descriptive way, it's

more didactic, but when you have a little time you

can...

Another character we're going to find

is the atrial natriuretic factor. You'll

find it in books as

Paul and atrial natriuretic peptides.

There's also an atrial natriuretic polypeptide

to find in the

literature, as well as a cerebral natriuretic factor

and another natriuretic factor that I can't remember right now,

and one in... Another material we're

going to

emphasize is atrial natriuretic factor, which is produced in

the atria. It's a

polypeptide that, when there's

atrial distension, the cells in

the atria will react and

release this atrial natriuretic factor into circulation. Its

site of synthesis is the cardiomyocytes,

which are the cells of the right atrium of

the heart.

To be more precise, its

action is the renal excretion of

sodium. It produces what are called

pressure natriuretics, meaning the

elimination of sodium when there's an

increase in blood pressure or an increase in

the volume of blood

reaching the atria. If the atria are

excessively distended, this atrial natriuretic factor is produced.

The mechanism is that when

there's atrial distension, in the case of

an increase in blood pressure,

the atrial natriuretic factor is released. This

increases diuresis, with an increase in the

amount of water excreted.

Sodium is eliminated, as we said, due to

pressure natriuretics.

Blood pressure and pressure are normalized because

plasma volume decreases.

The amount of fluid

in the blood decreases, leading to

water retention.

The production and effect of

angiotensin and aldosterone decrease.

Angiotensin and aldosterone, which both

inhibit

sodium elimination, promote

water elimination,

decrease sympathetic tone, and decrease

arterial tone. This is a renal effect,

therefore blocking

sodium resorption because sodium needs to be

eliminated. It inhibits

aldosterone secretion, as we've already mentioned,

and increases diuresis because sodium

draws water along with it. This

basically decreases

plasma volume because sodium and water are lost. It also has

the

opposite effect, inhibiting

the renin-angiotensin system and the

antidiuretic hormone. In other words, it

does the opposite because both the

renin-angiotensin system and the antidiuretic hormone

retain sodium and water, while atrial natriuretic

factor

eliminates sodium

and water through

urine.

Okay, so we're going to start talking a

little bit about what helps us with

the mechanisms for

concentrating urine.

Basically, the mechanism for excreting

excess solutes and

producing concentrated urine. For

this, you'll find that the

countercurrent mechanism is essential at the medullary level. First, let's

explain a little bit about what a countercurrent mechanism is.

The funnel fits

perfectly into the definition here.

A countercurrent mechanism of

tubules or vessels is created when, for

some distance, the

incoming fluid flow runs parallel to, or

against, the

outgoing fluid flow. That is, I

have a duct that carries fluid

upwards, and next to it, I have to

have a duct that carries fluid

downwards. That's basically the

countercurrent mechanism.

Some fluid flows upwards, and others

downwards, and they are in close relation, side by side.

A liquid countercurrent mechanism

is one in which fluid flows

through a long tube,

which would be

the loop of Henle, and the vasa recta with their

shadow in close proximity, so that

The exchange of

constituents can take place

between both branches, and what leaves one

can enter the other. This allows

for a high osmolarity in the

interstitial fluid of the renal medulla,

which is

an indispensable function and cannot be

lacking for the

concentration of urine. The hyperosmolarity

of the

renal medulla, especially

the innermost part, must

always be hypermolar. If we

cannot maintain this

hyperosmolar characteristic of the

medullary interstitium, what ends up

happening is that our body

will end up

eliminating all the solutes. We won't be

able to stop the flow because it's

there, but as life goes, we'll see

that it's very important to maintain this

system so

that not everything

in the blood is eliminated

via the bloodstream, so it ends up being

eliminated through the

urine. In summary, as a final result, we'll

see why

this countercurrent mechanism is

facilitated by the anatomical arrangement

of the loops of degenerated nephrons.

Medullary neurons, keep this in mind because

the others don't serve to concentrate

urine; they serve to produce urine

but not to concentrate it.

And of the vasa recta that these

medullary neurons had, here I'll go

back to slide 2, but the

axis is still stuck halfway, yes, and that's why the

countercurrent mechanism is where two

tubes run parallel, one

with the direction of the medulla downwards, the

other with the direction of the lithium upwards. They are

practically in close contact,

so what comes out of one branch can

enter the other. Yes, that's the

countercurrent mechanism, and of course it's

surrounded by the vasa recta because, we'll

see, what the vasa recta

do is a kind of

buffering of

osmolarity levels so that

all the solutes don't end up leaving through the veins, that is, so that

the washout, what

is called medullary washout, doesn't occur, and so that the

medulla remains hyperosmolar.

Well, requirements to eliminate concentrated urine:

first and foremost, that the

antidiuretic hormone is present, which we have already seen what it is for

and where it has its effect, and

second... Osmolarity in this case is

written from or modality but the same

the osmolarity of the medulla

and I'm inviting you to stop so you don't get scared, it

seems

complicated but it's not that much, it takes

time to digest it but as we said

this is going to be our

countercurrent mechanism, it will be formed

by a countercurrent multiplier

which will be part of the

loop of Henle and a

countercurrent exchanger which will be given by

the vasa recta, yes that's why

we said like a

buffer because you exchange and they keep

exchanging what happens in it

[Music]

in the tubular part, let's say of the sege,

here you have one, it's like

the proximal convoluted lobe would be up to, let me,

descending to the

distal convoluted ascending lobe and

collecting ducts, yes the collecting ducts have a

cortical part because remember

that the medullary part is in the

cortex and a medullary part, yes here you

have the net cut, from here up

is cortex and from here down is medulla, of

course the most correct ones are

Embracing what was in the path

of the angels, here we have it separated

so we can see what happens with the

electrolytes and with the solutes. Yes, well,

so what happens here

with the electrolytes and

the different solutes? Here, of course, it was

filtered.

If the blood

passes into the rubber capsule, in the urine, and

throughout the

proximal convoluted tubule and the thick descending limb,

there is a passage from the tubules to the

interstitium

by osmosis of water. Yes, so at

this level, as

the urine goes down towards

the deep part of the medulla, the

concentration becomes more concentrated because

water is being lost. Yes, so

look here, two modalities of

approximately 300. And as

we descend towards the deep part of

the medulla, the concentration increases;

the urine becomes hyperosmotic.

Yes,

water continues to come out here due to filtration and

because, remember, the interstitium is

hyperosmolar. So, by osmosis,

especially in the thin part of the

There are genes because, remember, the

thick part has cells that are

metabolically active. The thin part

is only prepared for

simple diffusion mechanisms; they

are not prepared for

active transport mechanisms because they are

not very active cells, and that's why they are thin. In

the thin part, if the cells are more

flattened, then

both continue to be lost, becoming

hyperosmolar as

the path of the amniotic fluid progresses.

When it reaches the

hairpin, it has approximately 1200

moles of osmolarity.

What happens when it turns around

the hairpin? Yes, we

have a lot of water.

Therefore, the sodium is concentrated

in this first part.

Remember that there was diffusion

in this part; it was only prepared

for diffusion.

This part immediately, when it

turns around the hairpin, sodium passes by

diffusion

to the outside, into the

interstitium, contributing to that hyperosmolarity. Notice

that everything that is a dashed line is

water; the

solid line, the black, is

sodium chloride;

in red, is the flow Blood that travels through

the vasa recta and the green area indicates the

presence of sodium,

potassium, and chloride transporters.

What does this mean? In this area, where

the green walls and green arrows are, these are

the areas where

sodium transport occurs. There is

active transport, yes,

because sodium has to be transported

against its concentration gradient. Sodium is transported

to the interstitium to maintain the

hyperosmolarity of the medulla.

Basically,

the

thick ascending limb of the loop of Henle maintains the hyperosmolarity of the medulla.

And, of course, as

sodium is sent to the

interstitium at the ascending level, the osmolarity

of the urine decreases as it

reaches the

cortex. What does this mean? That at the

medullary level, the urine will have a

higher osmolarity, and at the

cortical level, its osmolarity will decrease. That

is, the fluid that leaves

the tubules

will be a fluid with a

low osmolarity. If the

urine sample has an osmolarity of 300,

it will be less

than 300 compared to the cortical area. The

deeper part of the medulla, which can reach

1200,

always has a low polarity. The lithium that leaves the

tubule, the lithium that

is in the tubular part but is

part of the cortex, will have a

low polarity. In contrast, the part

that is in the medulla will have

an alpha polarity. This is because, as I

repeat, as

the fluid descends, it

loses water and concentrates sodium.

When it just returns to the hairpin,

sodium passes into the interstitium

and is then actively pumped by

transporters into the

medullary interstitium. Therefore, the sodium chloride concentration is

maintained, but the

medullary concentration is a characteristic that must be

maintained. Imagine

if all this sodium chloride didn't pass into the

interstitium; all this sodium chloride would be

lost in urine. If we didn't have

that mechanism of

urine exchange, what

happens is that the

countercurrent exchanger

also prevents

the medullary part from being washed away and

losing solutes.

Remember that the speed of

blood circulation in the cortex...

The speed at which

blood circulates through the

vasa recta is much higher than in the bone marrow. The speed at which blood circulates is very slow. Therefore, as

these vasa recta

descend, they absorb sodium chloride.

Yes, because remember, it becomes

hyperosmolar as you descend

deeper into the medulla.

So they absorb sodium chloride, and

the blood also becomes

hyperosmolar. But as the vasa recta

accompanies the ascending limb of the loop of

Henle, it loses

sodium chloride. Yes,

this causes it to lose sodium chloride

in the blood

circulating through the vasa recta. That's why

we said that it acts as an

osmolarity buffer, a

countercurrent exchanger.

Therefore, the blood that leaves

the vasa recta, notice that it leaves with

a flow rate practically the same as

the urine entering the collecting tubules.

This prevents the sodium chloride that

entered, at the

level of the

right angle, which is

deeper, from being lost as well.

The rest of the blood, then, what this does

is maintain, let's say, the

osmolarity and

solute concentrations in the medulla. If, in the medulla, CIF,

what happens if the speed at which

the blood flows here were fast, there wouldn't

be enough time for this

sodium chloride exchange to take place. We'll

explain later what

recirculation has to do with it, and this unit also

helps to make that renal medulla more

hyperosmolar. Yes,

and what will happen? It flows quickly and then

carries away all the extra

sodium, and back into the

general circulation, which we don't want

because what we want is to

retain sodium chloride if

necessary and lose it if

necessary. And the same with urea. Yes, Laure, well,

50% of

what is filtered is recirculated; only 50% is eliminated. If

the rest is recirculated, there are

exchanges between the vasa recta in

our sols, which are emitted up here, the

vasa recta and the renal tubules.

So this is basically what

the most important mechanism for that

hyperosmolar medulla does. Yes, and that

hyperosmolar medulla makes that

the salt urine in the bony part that

reaches the collecting duct is a urine

and I put the if it has a value of

300

dance let's see what

the hormones both antidiuretic us

theron a do with this liquid that leaves the

tubular system and passes to the collecting tubules

what e So, what happens with urea... notice

that urea... an area, however you want to call it...

notice where there's

circulation... you see, in this part, from this

part down, that is, in the

inner medulla, or in the deepest part of the

medulla, in the superficial part of the

medulla and in the cortex, there's no

recirculation. That's a detail

that only occurs in the

deep part of the medulla.

What happens here is that, while the urine is

filtered—

we'll see, as we

also mentioned last class—which part of

urea is very useful for acquiring... well, urea

isn't

an endogenous substance that would be very

useful for making tissues, because

urea is filtered, secreted, and reabsorbed. That

is, basically 50 percent

of what is filtered is eliminated.

But what happens to the urea? The urea is

remade. Can it be reabsorbed? We'll see

what situations: it's reabsorbed from the

deep cortical collecting tubules, it

passes into the interstitium, and in the

interstitium, what it does is help... It

also helps maintain urea levels because it's an

osmotically active substance,

meaning it contributes to hyperosmolarity. It

also

passes into the thin ascending limb of the

urea, which is why it's called

recirculation. Urea is

reabsorbed from the collecting duct, passes into the

interstitium, and also enters the

ascending limb.

Therefore, some of the urea will return to the

collecting duct to be reabsorbed, and

some will be eliminated in the urine. So,

seriously, here we have

half of the urea recirculation.

The urea is filtered;

100% of it remains. Some of it

goes

into the convoluted tubules,

and some

goes deeper into

the medulla.

This whole area, this part

with the thickest walls,

is completely

impermeable to urea. The

proximal convoluted tubule is slightly

permeable, as you can see here with the arrow.

The medulla is a little more

permeable. The descending part,

the part of the hairpin and the

thinner part of the ducts is

extremely permeable, and this part, that is, the

ascending tubule, the bulk of the system of people

and vital convoluted tubules, notice

that it has a thicker wall here, it is

totally impermeable to the

passage of urine. The same here,

where it becomes permeable again in the

part of the internal medulla of the collecting duct,

yes, of the collecting duct. So at this

level, it can, but there is

recirculation of urine, that is, from the part

of the internal collecting duct, it passes into the

interstitium, from the interstitium back into the

tubular system of the Angels. Therefore, there is

reabsorption and it is only eliminated little by little.

Yes,

when there is

a high amount of urine

in the blood, that is, there has to be

retention because this part, we will

see, is only permeable to water

when there is antidiuretic hormone. Yes, otherwise it

is totally impermeable

to water. Also, when there is release The

antidiuretic hormone reabsorbs water and

also stimulates

urea recirculation. If all this is to maintain

the hyperpolarity of the medulla,

then the mechanism for extending the

excess urine and excreting

concentrated urine is good. What this

diagram shows you is at the level of the collecting duct

near the sag in the descending blood-collecting loop of the loop of Henle.

If we already know how

the osmolarity changes, yes, as

that fluid passes through

the different sections of the loop of Henle,

what happens here? We had said

that when it was filtered it had a

polarity, a value of 300 moles

per liter. So in the

convoluted tubule near the loop of Henle, as it passes through

the different portions,

notice that the osmolarity increases,

reaching up to 1200 in

animals that concentrate their urine more.

This 1200 is even a higher value. Yes,

as it ascends again through

the loop of Henle, the

osmolarity decreases because here A

distal convoluted tubule, we're already back in the

cortex, meaning

the cortex always has a modularity. Okay,

what happens when there's antidiuretic hormone? When

there's antidiuretic hormone in the collecting duct, the

osmolarity will increase because it

will reabsorb water and

leave the solutes inside the

collecting duct. This is true as long as there isn't

20% natriuretic hormone, because if there's aldosterone, it

also retains the solutes.

This is only in the case where

we're only talking about

antidiuretic hormone. If there's antidiuretic hormone at the

level of the collecting duct, which is

totally impermeable to water, if it's not present,

water will be absorbed through those

aquaporin channels we saw earlier.

So the fluid becomes more concentrated.

If the osmolarity were rising again,

in this case we reach a

urinary density of approximately

1,000-30,050. Normally,

we humans eliminate urine with a density of 1,000-25,000-36,

but in In the case where we are

slightly dehydrated, it

can reach 56.

Okay, let's move on to the next one.

Here's the one that emits what

this critical shows. It's in the Gayton. What you're

going to see is in the different portions

of the tubule where there is

active transport of sodium chloride and where there is

positive or negative permeability in the

different portions. We'll see it

calmly if we go for an hour and

a half,

or try to cut at an hour and a half.

What happens, we said, in the

proximal tubule? In the proximal tubule, there was

active transport of sodium chloride, yes, that

is, there was a passage of sodium into the

interstitium.

What happens in the thin descending limb and the

final ascending limb? There is no active transport,

but what there is is a certain degree of

diffusion. When the tubule turns

in this part, there is some diffusion of

sodium chloride into the interstitium

because there is a high concentration in

the tubule, therefore it diffuses into the

interstitium, but only in that

small portion. What

happens in the thick ascending limb is that there is

active transport again,

but through a different mechanism.

In this case, it's X

with transport.

What happens in The distal tubule will

have transport from

sodium chloride. The cortical collecting duct and

medullary connecting duct will also have it, but

in this case it will depend on the

presence of hormones.

Here it says, here it shows you the little crosses,

a single little cross. Antidiuretic hormone:

permeability to water or urea increases

due to the presence of antidiuretic hormone. Yes, and

in this case, in the distal tubule and collecting ducts, it

depends

on the presence of aldosterone. Yes, it doesn't

clarify here, but if not, they are also

impermeable.

What happens in terms of

permeability? Of water, of

sodium chloride, and of urea? The next one is

permeable

to water. We said that there is

diffusion of water, and you see the little arrows

for sodium chloride. There is permeability

because there is active transport and diffusion.

There is also permeability because in the

first portion we said that there is a

certain degree of permeability. In the

thin descending limb,

the permeability remains the same for

water; that is, water passes by diffusion

because we are in a hyperosmolar interstitium. Now

we are in the medulla. So,

thin descending limb

Sodium chloride permeability is

slightly lower. If you saw that I

only mentioned where the hairpin bends, there is

permeability there.

Urea is permeable, of course,

because in the inner medulla,

and we had said that's where

urea recirculation occurs most to maintain

that hyperosmolar environment,

which is what happens with the thick ascending limb.

In terms of water permeability, it's

0 to 1.

The thin ascending limb is completely

impermeable to water. The thick ascending limb

is completely impermeable to water,

and remember that there was only

sodium chloride transport

to maintain the polarity of the

medulla,

and it is completely impermeable to urea. Yes,

well, let's continue with the distal tubule.

The distal tubule, in terms of permeability,

is permeable to water. Yes, there is, but it is

not completely impermeable

to sodium chloride. It is completely impermeable to

urea

because the distal tubule is in the

cortex. We had already said that in that

area of ​​the spinal cord, it is already impermeable

to urea. It was only permeable in the

deep medullary part. What

happens in the cortical collecting duct is that

water is only absorbed if there is

antidiuretic

sodium chloride. Sodium chloride is

completely impermeable unless you do

20 nat (if they don't clarify here),

and urea is also completely impermeable

because it's closer, it's in the cortex. What

happens with the internal medullary collecting duct? It's

permeable to water if we have

antidiuretic sodium chloride, completely impermeable to

sodium chloride, and

extremely permeable to urea, especially if there is

antidiuretic sodium chloride, which is what I was

telling you today when we saw that

image of the countercurrent mechanism.

When there is an antidiuretic, that

urea recirculation is enhanced; there is greater

reabsorption by the

collecting ducts, but not from the deeper part of the collecting

duct, not from the

more superficial part.

Well, up to here. From now on, we're going to see this

type of diagram where it shows a

tubular section, yes, and here it shows which

part this tubular section is from.

For example, here we are seeing a

cross-section of the

thick ascending limb where we had that

pumping action, that pumping action with

active transport of

sodium chloride. Interstitium, yes, well,

so what happens at

this level? There will be reabsorption, as the

photo shows here. The absorption of

sodium, chloride, potassium, calcium, bicarbonate,

and magnesium. Yes, there will be

secretion of ions

towards the lumen of the tubules.

Generally, we are close

to the cortex. Remember that's why

I did this and put

the osmolarity here. This was low; it's very

high here in this part and very low in

this part, and it's practically the same. The

osmolarity we will find in

the interstitium is high within

the tubules, coinciding with an

angular ridge in the interstitium. And being low in

the tubules near the cortex, there is

also a low polarity in the

interstitium of the cortex.

So, the thick ascending limb,

which we had said, and the

thick descending limb, when they are thick,

have a thick epithelium. Here,

25 percent of

solute reabsorption occurs. Remember that they are being

transported towards the interstitium.

There is also the presence of the sodium-

potassium pump and ATP synthase. They maintain

low intracellular sodium levels, meaning that while there is

transport from the lumen inwards, remember that, as we

discussed in the last class, at the

level of the basolateral membrane, there are

sodium and potassium pumps, and the one that acts in this way

is excreted. And remember,

those intercalated cells, which you will

see later, maintain the

blood's pH; it is one of the

buffer systems we have in the body. And

as we already said, one sodium

ion and one potassium ion are transported. If

sodium enters the cell from the lumen, this is

how sodium enters, and

potassium enters the cell. The

transport and counter-

transport mechanisms, remember, are in the

apical membranes of the

tubular cells, and how this sodium passes through, how it is

exchanged with the

interstitium through common

sodium and potassium pumps that are in the

lateral vessel membranes, on

the side facing the interstitium.

And it's the same with all of this. If you have

any doubts, if there is anything that was

n't clear, we didn't finish

clarifying it in the talk on Monday.

Here we see a section of...

Distal tubules and the

cortical collecting duct, more than anything here, what happens is that

sodium, chloride, calcium, and magnesium continue to be pumped into the interstitium or removed from the tubular lumen.

What happens in the

cortical collecting duct, the cortical symphysis, almost

entering the medulla, is that sodium and chloride will be

removed from the lumen of the tubule and

potassium will be pumped into the lumen of the tubules because

aldosterone is already acting here. Remember that

aldosterone retains sodium but doesn't

exchange it for potassium. What

will also happen here is that

the anti-aldosterone is active, therefore there will

be antibiotic-dependent water reabsorption.

If the antibiotic weren't present,

this area would be completely impermeable to water.

Bicarbonate ions will also be removed from the lumen of the tubule to retain

sodium because bicarbonate is being retained,

and fluoride will also be secreted,

and

hydrogen ions will be secreted. Remember that we

also have intercalated cells,

as it says here, which are the ones that maintain

the pH. Therefore, this terminal portion

of your list, the

distal convoluted tubule and collecting duct, has the

same characteristics. Yes,

water reabsorption, which is the

most important thing, is controlled by

the concentration of antidiuretic hormone. If there is no

antidiuretic hormone, nothing is reabsorbed.

Sodium enters through cells via

special channels. It will also

depend on aldosterone, and the

intercalated cells secrete

hydrogen ions and reabsorb bicarbonate and

potassium.

Let's look at the cross-section

of the function of the external medullary collecting duct.

Here we have medullary,

more than external medullary. Here I think I'm

mistaken about external and

internal medullary collecting ducts.

What happens here is that

sodium and chloride are reabsorbed. If there is

aldosterone, water is reabsorbed. If there is

any antidiuretic hormone, there is

urea recirculation, especially if there is antidiuretic hormone; there will be

more urea recirculation.

Reabsorption of bicarbonate ions

and there will be secretion of hydrogen

ions by the intercalated cells

because in some places it seems that

sodium bicarbonate comes out, in others that it

comes in when there is hydrolysis because there has to be

an exchange of

bicarbonate ions, that is, if I want to

alkalize the internal environment I need to

remove hydrogen ions and

put in carbonate ions, yes, and also

sodium. So in that way he managed to

alkalize the cells of the

medullary collecting duct. They have a role in the

binary concentration. If it is impermeable

to water under basal conditions, but if there is

antidiuretic hormone, it is extremely

permeable.

Permeability increases by the insertion

of type 2 choline water channels in

the membranes.

And we move on to the next

mechanism of elimination of excess

water: formation of dilute urine. This is

much easier because what is

the only thing that has to happen here is that

antidiuretic hormone is not secreted if the

urine is filtered. These are diagrams,

but what happens is that the

urine is filtered. It would go from 300, of course it will

increase because the

interstitium will always be

hyperosmolar here. The same thing that happens

in the countercurrent mechanism involves

sodium transport, creating interstices

to maintain the

interstitial fluid.

This is what makes the difference between what

happens here and in the rest of the

collecting tubules. Yes, if I need to

form dilute urine, what happens

is that the release of antidiuretic hormone is blocked.

So this whole area

becomes completely impermeable to water.

Then all the water that enters the

collecting duct is eliminated. Yes,

and what must be present is

aldosterone to avoid losing excess

solute along with the urine. Yes, then there is

reabsorption, basically of

solutes, yes, and sodium and

chloride ions as well, because there are 22 together. Yes, so

that's the only difference. It's

more complicated to eliminate

concentrated urine than to eliminate daytime urine. This

would be

like the final conclusion

regarding concentration and the division of

matter.

Well, here, the same thing we saw in the

previous diagrams,

but for the

formation of dilute urine, it is filtered

through the glomeruli and the

convoluted tubule. A polarity of

300 million moles as it passes through

the different segments

of the loop of Henle increases the

osmolarity in the deepest part of the

medulla,

and as it works in the

cortex it becomes a little more like a

schoolgirl,

yes, because water needs to be eliminated.

If there is aldosterone, the

amount of solutes is retained, yes, and if there is no

antidiuretic hormone, of course,

all the fluid that enters the

distal convoluted tubule and collecting duct is eliminated.

Therefore, urine with a

density much closer to the density of

water is eliminated. Without the density of water being

1000, we can eliminate urine

very similar to water, up to 1000.5, so

this process is much

simpler, the process of formation of concentrated urine.

Now we move on to what is the

medullary apparatus, which we had said we would

talk about at length. You will see

that the medullary apparatus is

formed when the tubule in the

thick ascending limb of the loop of Henle

transforms into the distal convoluted tubule.

This intersection makes contact With the

area of ​​the frontal artery and vas deferens, it

continues to inform what the

Shushtar apparatus in the medulla oblongata has.

What functions does it have? It's a

receptor organ. We'll see that here it

reacts, yes, and it's an

endocrine organ. Why? Because it

triggers the renin-

angiotensin-aldosterone system. It will have a

homeostatic function because it will

end up regulating the levels of sodium

and water in the body. It regulates

blood pressure and it regulates the

orthostatic reaction, the autostatic reaction

that occurs, for example, when an

individual is

sitting or lying down for a long time, or

when they have slightly

low blood pressure and suddenly stand up, and it's as if their blood

pressure rises or falls; some even feel

nauseous. This is the orthostatic reaction.

This apparatus, as we know it in the medulla oblongata,

largely prevents these

abrupt changes in pressure resulting from this

orthostatic reaction.

If you hear some

hammering nearby, it's because they're fixing

the apartment.

With this information, I wouldn't try to say it's

not noise, but anyway,

and what do we see here? Here we see

that half of what is the

glomerular apparatus, where we find

the thick ascending limb where the

distal convoluted tubule transforms.

These cells will be modified and are

the cells that form the macula densa,

which are

sensory cells. What these cells will detect is

whether the fluid arriving in this

area is more concentrated or more dilute, that is, if it

has a greater or lesser amount of

solutes.

And they make contact in the area

with the two arteries, but the

anterior one,

the anterior part of the artery wall, the

anterior part, will have

modified cells called

medullary stapes cells. These medullary stapes cells

produce renin.

This is called, of course, as we

had said, the macula densa. And the

cells that are filling it in, which

actually also have a

sensory function, a certain degree of phagocytosis,

are the Sanyal cells. These are

essential cells, which you will

find even among all the tufts

of capillaries, and which have the function of

nutrition, phagocytosis, and sensitivity for

various purposes. These cells have functions that are

good, as we

had said, that

the core issue is whether they produce

renin,

but renin has to have an effect on the

world, and

if renin has to have an effect

on a... If that substrate is going to

be the angel in silicon in general, and

those seven exist, but where does

that vision come from? It doesn't come from the

liver. The liver produces

an alpha 2 niko hepatic protein of

452 amino acids, the synthesis of

angiotensin, which is not going to be

stimulated by corticosteroids,

estrogens, T4 thyroxine, which is one of

the thyroid hormones, and angiotensin

2. Yes,

here we have the answer to why the

uncertain angiotensin 2 ends up regulating a

lot of other things that we're going to see.

Well, here we see how the angiotensinogen cycle is

and how that

apparatus works. There's the medullary part,

what happens here? If

the urine is filtered, of course,

there is a

release of renin by the

apparatus. It's from the cells, not the

lares.

The renin is going to transform the air or

foreign tenzin that is produced by the

liver, it transforms it into the vision. Angiotensin

one is transited. Angiotensin one doesn't have

any particular effect,

but I'm talking about angiotensin one when it passes

through the In the lungs, there's

a substance called

angiotensin-converting enzyme (ACE),

and this enzyme

transforms

angiotensin into a large, two-

stage angiotensin. This is very potent

because it produces

marked vasoconstriction, not

very long-lasting, but very powerful,

especially in the

arterioles.

As we mentioned earlier, this

triggers the

thirst reflex in the nervous system, causing

the individual to seek water. It

directly stimulates the

adrenal cortex to produce

aldosterone and

corticosteroids. These corticosteroids, at the

tubular level, produce

a reabsorption of sodium and chloride,

the creation of potassium,

and the excretion of hydrogen ions. In this

way, the entire system

helps to increase blood pressure

because it

reabsorbs sodium from the tubules,

preventing sodium loss and

thus increasing the amount of sodium in the blood.

of sodium, and if it's accompanied by

fluid intake and

fluid retention,

if there's antidiuretic secretion, what I

do is increase blood pressure,

but what I also do is maintain

fluid, that is, maintain water and

maintain water reabsorption, that is,

the amount of fluid in

our body, as you'll see,

is directly

related to blood pressure levels.

This basically explains the same thing,

but it's more complicated, and on

top of that, it's in a human. But basically, what this

is showing you—

let's look for where the kidney is—

what it tells you here is what

happens when there's low

blood pressure. When there's low

blood pressure, as a response to the reduction

in blood pressure or decrease in

sodium in the renal tubules, since that's

the signal that those cells of the maculae pick up,

the apparatus is in the medulla of the kidney. It

produces renin, and the discharge into the

bloodstream, renin, as we already

said, let's see here where they are

[Music]

renin

will transform the laziotetensinogen, or

if the renin is discharged The thirst changes;

here's where renin

transforms angiotensinogen into

angiotensin I, which we said

wasn't potent and had no effect at the

vascular level. This, I mean, angiotensin I,

travels through the bloodstream to the lungs and

through the ACE (this is in English, that's why you're talking about the

ACE). It converts

angiotensin II, transforms it into zinc, and it's going

to circulate

through the blood vessels. Yes, and at the

nervous system level, it stimulates

thirst and stimulates the production and

release of antidiuretic hormone.

Yes,

and it's going to produce it for the

construction of blood vessels.

Its construction, vasoconstriction

of the blood vessels, will

decrease

circulation, increase the volume of

extracellular fluid, and increase

blood pressure. Yes, because it's

vasoconstriction, therefore it

increases blood pressure, but what it also does

is increase the amount of

fluid because it stimulates the

thirst reflex and stimulates the release of

antidiuretic hormone. That's why the hormonal axis

from this entire arterial-

renal part is called the renin-angiotensin-aldosterone system.

Angiotensin, aldosterone, and antidiuretic hormones—

if when one starts

to be produced, they all start to be produced, that's why

the hormonal axis is made up of

all those substances. I'll

repeat it: renin,

angiotensin, aldosterone, and antidiuretic hormones. Yes, they

always act together.

And lastly, I think this is the

last thing so it doesn't look too

cartoonish. If we repeat, there are

some concepts that need to

be firmly established. When there's a drop in

blood pressure,

these are the kidneys.

When there's a drop in blood pressure,

from the glomerular apparatus, if

the enzyme is released—because it's a key enzyme—it

will transform the line, well, it's not that

the little bit that's useless, that

's in an inactive form, into

something a little

different, which is

angiotensinogen,

angiotensinogen-converting enzyme. Yes,

but it has to go

to the lungs

to meet the

angiotensin-converting enzyme. Yes, and

so they're fine, but not the one that

appears here as a chubby little thing, and that... As

soon as it moves, it transforms into this

super-powerful enzyme, the restless enzyme

2. Yes, there is a

certain enzyme 2. It produces

vasoconstriction, and it directly stimulates

the adrenal gland to

release aldosterone. These two hormones are

released into the circulation, and what it ends up

doing is excreting

potassium through the tubules and

retaining sodium. If the sodium is retained

and passes into the circulation, for example, through

sex, that's all that happens

in the interstitium. It's because it later ends up

passing into the aldosterone system,

and it passes into the blood. So this sodium,

which is like a salt shaker in the brain,

plus the salt and sodium, also, as

we said, stimulates

the release of antidiuretic hormone, also

retains water. It retains water through

the tubules and passes it into the circulation, and it

also stimulates the central nervous system so that

the individual seeks

water and incorporates water to help, of

course, with kidney function. Because if

we don't incorporate water, our

kidney will continue to produce, I

repeat, that obligatory volume

of urine to

eliminate waste. And that it will end up

dehydrated, so it's

a combination of retaining sodium,

retaining water, and also

seeking and incorporating fluids. While it's true

that fluids are

n't only lost through urine, they're

also lost through feces, through

sweating (in animals that sweat,

which isn't all of them), through

evaporation, and through respiration, meaning

fluid is lost over many

days, not only through the kidneys.

Therefore, fluid incorporation is

extremely important. Well, I hope that's

clear. If it's not, I

know that the most complicated and

difficult part to process is the

countercurrent mechanism. We'll

see you next Monday. I hope you have your

questions written down so we can

work more quickly. And of course,

share the link with your classmates

so there are more of us at the meeting.

Well, greetings and take care, and see you next time.