The Renin-Angiotensin-Aldosterone [RAAS] Pathway EXPLAINED
Summary
TLDRIn this Catalyst University video, Kevin Tockoff delves into the Renin-Angiotensin-Aldosterone System (RAAS), a crucial pathway in health disciplines. He explains how RAAS functions as a negative feedback loop to regulate blood pressure, starting with the release of renin in response to low blood volume or pressure. The video covers the conversion of angiotensinogen to angiotensin II by the lungs' ACE enzyme, which then stimulates aldosterone production to increase blood volume and pressure. Tockoff also touches on the role of angiotensin II in vasoconstriction and hints at upcoming discussions on related medications.
Takeaways
- 🔬 The RAAS system stands for Renin-Angiotensin-Aldosterone System and is a key pathway in health disciplines to regulate blood pressure.
- 🌀 The initial stimulus for the RAAS system is a decrease in blood volume or blood pressure, which triggers a negative feedback loop to raise blood pressure.
- 🧬 Juxtaglomerular cells in the kidney release the enzyme renin in response to low blood pressure, initiating the RAAS pathway.
- 🏗️ Renin acts on angiotensinogen, an inactive protein produced by the liver, converting it into angiotensin I, a peptide hormone.
- 💨 Angiotensin I is converted into angiotensin II by the angiotensin-converting enzyme (ACE) in the lungs, which is the active form of the hormone.
- 🚀 Angiotensin II stimulates the adrenal cortex to produce aldosterone, which acts on the kidneys to increase sodium and water reabsorption, thereby raising blood volume and pressure.
- 🔄 The reabsorption of sodium and water due to aldosterone leads to an increase in blood volume, which in turn increases blood pressure, completing the negative feedback loop.
- 🌡️ Angiotensin II also causes vasoconstriction of arterioles, directly increasing blood pressure by constricting blood vessels.
- 💊 Medications such as ACE inhibitors can interfere with the RAAS pathway, providing a method to treat blood pressure issues.
- 🛠️ The understanding of the RAAS system and nephron structure is crucial for comprehending the mechanisms of action of various blood pressure medications.
- 📚 The video promises to cover more on the inhibition of the RAAS pathway and other medications in a subsequent video, highlighting the importance of continued education on the topic.
Q & A
What is the primary function of the renin-angiotensin-aldosterone system (RAAS)?
-The primary function of the RAAS is to regulate blood pressure and blood volume through a negative feedback loop, increasing blood pressure when it is decreased due to low blood volume.
How is blood volume related to blood pressure?
-Blood volume and blood pressure are directly proportional. When blood volume is low, blood pressure is also low, and vice versa.
What is the role of the juxtaglomerular cells in the RAAS?
-Juxtaglomerular cells, located in the kidney, sense decreased blood pressure and release an enzyme called renin into the blood, initiating the RAAS pathway.
What is renin and why is it not considered a hormone?
-Renin is an enzyme, not a hormone, that is released by juxtaglomerular cells in response to low blood pressure. It acts on angiotensinogen to convert it into angiotensin I.
What is the role of angiotensinogen in the RAAS?
-Angiotensinogen is an inactive protein produced by the liver. It is converted into angiotensin I by the action of renin, which is a crucial step in the RAAS pathway.
How does angiotensin II affect blood pressure?
-Angiotensin II is a peptide hormone that acts on the adrenal cortex to stimulate the release of aldosterone and causes vasoconstriction of arterioles, both of which increase blood pressure.
What is the function of aldosterone in the context of the RAAS?
-Aldosterone, released in response to angiotensin II, acts on the kidneys to increase sodium and water reabsorption, leading to an increase in blood volume and blood pressure.
How does the reabsorption of sodium by aldosterone affect water levels in the blood?
-The reabsorption of sodium by aldosterone leads to water following the sodium due to osmosis, resulting in increased blood volume.
What is the significance of the collecting duct in the nephron in the context of the RAAS?
-The collecting duct in the nephron is where aldosterone acts to increase sodium reabsorption and water reabsorption, which in turn increases blood volume and blood pressure.
How do angiotensin-converting enzyme (ACE) inhibitors work in relation to the RAAS?
-ACE inhibitors are drugs that block the conversion of angiotensin I into angiotensin II by the angiotensin-converting enzyme, thus reducing the effects of the RAAS pathway and lowering blood pressure.
What are some potential causes of decreased blood volume that could trigger the RAAS?
-Decreased blood volume can be caused by severe dehydration, sodium deficiency, or bleeding episodes, all of which can trigger the RAAS to restore blood pressure.
Outlines
🛡️ Renin-Angiotensin-Aldosterone System (RAAS) Overview
This paragraph introduces the Renin-Angiotensin-Aldosterone System (RAAS), a crucial pathway in health disciplines for regulating blood pressure. It explains that the system is activated by low blood volume or pressure, which triggers a negative feedback loop to increase blood pressure. The initial stimulus could be due to dehydration, sodium deficiency, or blood loss. The paragraph details the role of the juxtaglomerular cells in the kidney, which release the enzyme renin when they sense decreased blood pressure. Renin acts on angiotensinogen, an inactive protein produced by the liver, converting it into angiotensin I, which is then converted into the active hormone angiotensin II by the angiotensin-converting enzyme (ACE) in the lungs. Angiotensin II is a key component of the RAAS, responsible for several functions that contribute to blood pressure regulation.
🌀 The Role of Aldosterone and Angiotensin II in Blood Pressure Regulation
This paragraph delves deeper into the functions of aldosterone and angiotensin II within the RAAS. Aldosterone, produced by the adrenal cortex in response to angiotensin II, increases the reabsorption of sodium in the kidneys, leading to increased water reabsorption and thus higher blood volume and pressure. The paragraph also explains the role of specific proteins in the collecting ducts of the nephron, which facilitate sodium reabsorption and the secretion of potassium and hydrogen ions into the urine. Additionally, angiotensin II is highlighted for its ability to cause vasoconstriction of arterioles, directly increasing blood pressure. The paragraph concludes by summarizing the RAAS's role in normalizing blood pressure from decreased levels and hints at the discussion of medications that can influence this system in future videos.
Mindmap
Keywords
💡Catalyst University
💡Ras System
💡Negative Feedback Loop
💡Juxtaglomerular Apparatus
💡Renin
💡Angiotensinogen
💡Angiotensin Converting Enzyme (ACE)
💡Aldosterone
💡Nephron
💡Vasoconstriction
💡Thiazides and Loop Diuretics
Highlights
Introduction to the Renin-Angiotensin-Aldosterone System (RAAS) which is crucial for maintaining blood pressure.
Explanation of the negative feedback loop in the body that raises blood pressure when it's decreased.
The relationship between low blood volume and low blood pressure, and the causes of decreased blood volume.
The role of the juxtaglomerular cells in the kidney and their release of the enzyme renin in response to low blood pressure.
Clarification that renin is an enzyme, not a hormone, and its function in the RAAS pathway.
The liver's production of angiotensinogen, an inactive protein, and its conversion to angiotensin I by renin.
The function of the angiotensin-converting enzyme (ACE) in the lungs to convert angiotensin I into angiotensin II.
Angiotensin II's role as an active peptide hormone with multiple functions in the body.
How angiotensin II stimulates the adrenal cortex to produce aldosterone, a hormone that affects blood pressure.
Aldosterone's direct action on the kidneys to increase sodium and water reabsorption, thereby raising blood volume and pressure.
The structural overview of the nephron and the specific location of aldosterone's action in the collecting ducts.
The mechanism by which aldosterone increases the reabsorption of sodium and water, leading to increased blood pressure.
Angiotensin II's additional function of causing vasoconstriction of arterioles to increase blood pressure.
The collective effect of renin, angiotensin II, and aldosterone in the RAAS system to regulate blood pressure.
Potential issues with blood pressure regulation and the role of medications in treating blood pressure disorders.
Introduction to the use of different medications acting on various parts of the nephron to manage blood pressure.
Upcoming discussion on the mechanisms of action of various drugs for treating blood pressure in relation to the RAAS system.
Transcripts
welcome back to catalyst university my
name is kevin tockoff
please make sure to like this video and
subscribe to my channel for
future videos and notifications and a
big thank you to my patrons on patreon
for your contributions to my channel
in this video we're going to be
discussing a very important pathway in
any health discipline
whether it's medicine physical therapy
or whatnot
and that is what's called the ras system
you can see the raas
here in the title of the video and what
it stands for is
renin angiotensin aldosterone system
and what this system allows for is when
the body
has a decreased blood pressure it allows
a negative feedback loop to raise the
blood pressure and that's what we would
expect from a negative feedback loop
right if we have some initial stimulus
well the outcome should be
moving that parameter in the opposite
direction so let's start up here at the
initial stimulus and work our way
through this complex looking diagram
and hopefully you'll see that it's
actually not very complicated it
actually makes a lot of sense
our initial stimulus is going to be
either low blood volume
or low blood pressure now one thing to
understand is that
whenever the blood volume is low that
always means we have a low blood
pressure these two things are
proportional to one another
if the blood volume were high the blood
pressure would also
be high but our initial stimulus is low
blood volume and there could be a number
of things that caused this
we could have some severe dehydration
maybe we were in the desert too long and
we haven't consumed any fluids
we could have a sodium deficiency
remember water follows salt so if we
have low sodium
we also have low water content or it
could be a bleeding episode where we're
hemorrhaging and losing blood and
therefore losing blood volume
so whenever we have that decrease in
blood volume that's automatically going
to mean we have a decreased blood
pressure those two things
always go together now within the kidney
we have a cluster of cells
referred to as the juxtaglomerular
apparatus and within that apparatus
there are some cells
that are called juxtaglomerular cells
often called jg cells for short
now when these jg cells sense this
decreased blood pressure they release an
enzyme into the blood this enzyme is
called renin
now one thing about renin this is not
important for the function of the ras
pathway but
you might see in some sources they'll
refer to this as a hormone
renin is not a hormone it is an enzyme
and we'll see that in just a minute
now coming over here to the liver the
liver manufactures many proteins one of
which is angiotensinogen
this is an inactive protein and it does
nothing right now
it's in your blood circulating as we
speak anytime you see the suffix inogen
or ogen that implies that the protein is
in an inactive form so
the liver makes it but there's always
some level of angiotensinogen
in your blood right now it's just not
doing anything
but let's suppose that these jg cells
release renin into the blood
and it acts on angiotensinogen and
converts it into angiotensin one
which is a peptide that circulates in
the blood now
circulating the blood eventually
angiotensin 1 is going to reach the
lungs because of course there's blood
flow that goes through the lungs
and there's an enzyme in the lungs
called ace
which is angiotensin converting enzyme
you might have heard of an ace inhibitor
that would be a drug that inhibits this
enzyme and we'll be covering more
on inhibition and other medications in
the next video once we understand this
but when angiotensin one gets to the
lungs ace
converts it into angiotensin ii
that makes sense based on this name it's
an angiotensin converting
enzyme it converts angiotensin one into
angiotensin
ii now angiotensin ii is the active or
the mature
form of the angiotensin hormone so
angiotensin ii is a peptide hormone
that's going to have several functions
coming over here one of these functions
is to act directly
on certain cells of the adrenal cortex
now the adrenal cortex makes many
hormones but one of them that's
important
is the hormone aldosterone so when
angiotensin
ii acts on specifically the cells of the
zona glomerulosa
of the adrenal cortex it triggers them
to dump aldosterone
into the blood now aldosterone is able
to act
directly on the kidneys specifically
in the collecting ducts of the nephron
okay so let's actually go to this
picture we'll look at this more
in another video when we talk about
these drugs but i want you to look at
the general structure of the nephron
up here we have the glomerulus then
here's the proximal convoluted tubule
and then here's my big loop of henle so
this part would be the descending loop
here's the ascending loop
then i have the distal convoluted tubule
and then over here
the terminal part of it is the
collecting duct
now you'll notice there's a protein
right here it's this yellow protein
and these proteins are specifically
found in the collecting duct cells
and what they do is they facilitate
reabsorption of
sodium into the blood okay so when
sodium is reabsorbed into the blood
water follows that sodium remember our
key here
water follows salt so the more sodium
that i reabsorb the more water that's
going to osmose through
and follow it okay
also this protein facilitates the
secretion
of potassium ions and hydrogen ions into
the filtrate which eventually go
into urine so we get rid of or excrete
potassium and hydrogen ions
now here is aldosterone usually
abbreviated aldo
now aldosterone actually up regulates
this protein
meaning when there's more aldosterone we
get more of this
transporter and if there's more of this
transporter
we reabsorb more sodium and we reabsorb
more water we also end up excreting more
potassium
and excreting more hydrogen ions
so coming back here if i have more
aldosterone what's going to happen to
the amount of water reabsorption
there's more water reabsorbed into the
blood therefore there's a greater blood
volume
and if there's a greater blood volume
what did we say that translates to
a greater blood pressure so our initial
stimulus back over here
was decreased blood volume and decreased
blood pressure our
outcome is increased blood volume and
increased blood pressure so this is a
great example
of a negative feedback loop where we
reverse the direction
of the original stimulus
now back to angiotensin ii here we've
been talking about aldosterone
but angiotensin ii has another function
and what it's actually able to do is
cause vasoconstriction of arterioles
so basically constricting blood vessels
and what do we know about blood vessel
constriction in the periphery
well when you constrict blood vessels
their diameter
decreases and so blood pressure in that
region will
increase and so angiotensin ii is able
to act directly
on the arterioles that lead to capillary
beds and
cause vasoconstriction which causes the
blood pressure
to go up so not only can aldosterone
independently of angiotensin ii increase
blood pressure
but the angiotensin ii can directly act
on the arterials to vasoconstrict them
which also increases blood pressure
and so this is the basis of the ras
system we have renin angiotensin ii and
aldosterone
and collectively they can take a
decreased blood volume and decrease
blood pressure and they can
increase it to normal levels now
obviously in some cases blood pressure
gets out of whack
and the blood pressure can get out of
whack for a couple of reasons one
can be independent of blood volume or in
another case it can be
with increased blood volume and so
there's different ways that we can
decrease blood pressure using
medications and so some of those
medications
act on different portions of the nephron
you can see that the thiazides act here
at the distal convoluted tubule
loop diuretics act somewhere on the loop
of henle
we're not going to cover that in this
video that will actually be the next
video
and so we'll use our understanding of
the ras system
and the nephron to understand the
mechanisms of actions
of the various drugs to help treat blood
pressure so make sure to join us in that
video
please make sure to like this video and
subscribe to my channel for future
videos and notifications
thank you
تصفح المزيد من مقاطع الفيديو ذات الصلة
Renin-Angiotensin-Aldosterone System (RAA System) | Made easy with a step-by-step explanation!
Hypertension medications that affect the RAAS system - Pharmacology - Cardiovascular | @LevelUpRN
Pharmacology - HYPERTENSION & ANTIHYPERTENSIVES (MADE EASY)
Blood volume physiology||blood volume regulation||measurements of blood volume
Sistema Excretor/Urinário: Aula 1/2. Anatomia e Fisiologia Renal
Blood Pressure
5.0 / 5 (0 votes)