The Renin-Angiotensin-Aldosterone [RAAS] Pathway EXPLAINED

Summary

In 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

00:00

🛡️ 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.

05:01

🌀 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.

Keywords

💡Catalyst University

Catalyst University is the educational platform where the video is hosted, presumably offering courses or content on health-related disciplines. It is the setting for the video, where the host, Kevin Tockoff, introduces the topic and engages with the audience.

💡Ras System

The Renin-Angiotensin-Aldosterone System (RAS) is a key concept in the video, describing a biological pathway in the body that regulates blood pressure. It is essential for understanding the video's theme, as it is the main subject being discussed and analyzed throughout the script.

💡Negative Feedback Loop

A negative feedback loop is a biological mechanism that helps maintain homeostasis by counteracting changes. In the context of the RAS, it is the process by which the body responds to low blood pressure by increasing it, as explained by Kevin Tockoff.

💡Juxtaglomerular Apparatus

The juxtaglomerular apparatus is a cluster of cells within the kidney that plays a crucial role in the RAS by sensing changes in blood pressure and triggering the release of renin. It is an important anatomical feature in the script's explanation of how the RAS initiates its response.

💡Renin

Renin is an enzyme released by the juxtaglomerular cells in response to low blood pressure. It is not a hormone, as clarified by the script, and is the first active component in the RAS pathway, initiating the conversion of angiotensinogen to angiotensin I.

💡Angiotensinogen

Angiotensinogen is an inactive protein produced by the liver that is converted into angiotensin I by the action of renin. It is a precursor in the RAS and is central to the script's explanation of how the system responds to low blood pressure.

💡Angiotensin Converting Enzyme (ACE)

ACE is an enzyme found in the lungs that converts angiotensin I into angiotensin II. The script mentions ACE inhibitors as a class of drugs that can affect this conversion, tying the concept to both physiology and pharmacology.

💡Aldosterone

Aldosterone is a hormone produced by the adrenal cortex that is triggered by angiotensin II. It plays a key role in the RAS by increasing sodium and water reabsorption in the kidneys, thereby increasing blood volume and blood pressure, as detailed in the script.

💡Nephron

The nephron is the functional unit of the kidney, involved in filtration and reabsorption processes. The script uses the structure of the nephron to explain where aldosterone acts to increase blood volume and pressure, illustrating the physiological impact of the RAS.

💡Vasoconstriction

Vasoconstriction refers to the narrowing of blood vessels, which increases blood pressure. In the script, angiotensin II is described as causing vasoconstriction, directly contributing to the increase in blood pressure regulated by the RAS.

💡Thiazides and Loop Diuretics

Thiazides and loop diuretics are types of drugs mentioned in the script that act on different parts of the nephron to decrease blood pressure. They are part of the broader discussion on how medications can be used to intervene in the RAS pathway.

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