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Renin-Angiotensin-Aldosterone-System (RAAS) (Nursing)

by Rhonda Lawes

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      Slides 06-01 Hypertension RAAS - ACE Inhibitors - ARBs.pdf
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    00:01 Now, you have this really cool diagram in your notes. I want you to take a look at it.

    00:06 It shows you where all the players of the RAAS. What organs they come from, what comes from the liver, what comes in from the juxtaglomerular cells, what comes from the lungs, what happens in the capillaries and what happens -- It's really neat.

    00:19 So I want you to pause the video for a second.

    00:21 Just take a look at it, orient yourself to that picture, and then restart the video when you're ready.

    00:34 Now let's break the RAAS down very simply. Okay, some reason your body senses, "Wow, we need to raise the blood pressure." Maybe it senses a drop in the blood pressure, maybe it senses a low sodium.

    00:49 Whenever that alarm bell goes off, the juxtaglomerular cells in the kidneys. Now, you may not be proud of me for saying that, but that word scares me to death every time I have to say it; juxtaglomerular cells, so I'm pretty impressed that I got it out.

    01:05 But renin is excluded from these j cells in the kidney because, why? The body sensed a need to raise blood pressure.

    01:15 So that's why renin -- that's squirted out through your kidneys.

    01:21 Now, renin connects up with circulating angiotensinogen.

    01:26 When you're looking at your downloadable section, where does angiotensinogen come from? What liver-colored organ does angiotensinogen come from? When renin and the circulating angiotensinogen meet up, you end up with a different product: angiotensin I.

    01:45 Okay, so I went from renin to circulating angiotensinogen. Well, why did the renin appear? Because my body sensed I needed to raise my blood pressure.

    01:55 So, renin connected to the circulating angiotensinogen, I end up with angiotensin I.

    02:02 Now, when angiotensin I meets ACE, or angiotensin-converting enzyme, you end up with -- angiotensin II.

    02:17 This is another bad mama jama.

    02:20 This causes potent vasoconstriction and volume expansion.

    02:26 So, the RAAS is a system -- 1 of the 5 key players that my body uses to maintain blood pressure.

    02:35 The renin -- Can you remember the reason that renin appears? Why does the body put that out? Why do those j cells in the kidney, put out renin? Renin connects with angiotensinogen, then you end up with angiotensin I.

    02:53 Angiotensin I hits ACE, angiotensin-converting enzyme pretty cool name, right? And you end up with angiotensin II.

    03:02 The end result of angiotensin II, my blood pressure is raised 2 ways, with a -- potent vasoconstriction and -- volume expansion.

    03:13 So what does that mean? That reminds me of that little girl in Willy Wonka.

    03:16 Remember when she said, "I want it now." She was the blueberry girl and she -- that volume blew right up, so that's why I'll use that to remind you.

    03:25 So look at the breakdown on the bottom of your screen.

    03:28 Why are we going over this over and over again? Because that's a great study tip for you.

    03:34 Repetition really helps your brain remember things.

    03:37 It likes to see things that it's familiar.

    03:40 So, renin plus angiotensinogen equals angiotensin I.

    03:47 Then angiotensin I connects with ACE and you end up with angiotensin II.

    03:53 Now there's 2 ways the release of angiotensin II raises your blood pressure.

    03:58 Can you remember the 2 ways -- and you don't have to do the sound effects -- but remember the 2 ways that angiotensin II raises your blood pressure? Okay, so we're not done with this. We're going to keep going over and over this concept because this is the key to understanding multiple high blood pressure medications. Okay? Just understanding how the RAAS works will make it so much easier for you to understand these types of medications. So, the 2 reasons that your blood pressure elevates because of the end product of RAAS angiotensin II, are volume expansion and vaso constriction.

    04:40 Now, you know the sound effects that go with that, right? Vasoconstriction and -- volume expansion.

    04:48 Now, the volume expansion comes from aldosterone.

    04:53 The adrenal gland releases aldosterone.

    04:57 Now, why would I say it like that? Because most normal people don't say aldosterone.

    05:03 1, it's pretty annoying, and 2, it's something you didn't expect and will help it stick in your brain better.

    05:10 So, while you don't have to agree with the way I do things, anything you can do while you're studying that makes something stick in your mind, then you'll say aldosterone. I remember that.

    05:22 I can be in the mall, and I'll meet somebody who I had 10 years ago in Pharmacology and they'll say, "Hey, Prof. Lawes, aldosterone," and I think, "Yes." So anything that's weird or unexpected that helps you remember information, go with it.

    05:39 You might not want to say it in public, but it'll definitely work in your studying.

    05:43 So when the adrenal gland releases aldosterone, that means the body hangs on to sodium. Those kidneys will hang on to sodium, and you know the rule.

    05:54 Wherever sodium goes, water follows.

    05:58 So, volume expansion comes from the release of aldosterone.

    06:03 That means the body hangs on to sodium, and wherever sodium goes, water follows.

    06:09 Now, the vasoconstriction that comes from angiotensin II, it is a very, very potent vasoconstrictor.

    06:17 Like, 4-8 times as active as norepinephrine.

    06:22 Norepinephrine is a drug that we use usually in the critical care setting for someone who is desperately, life- threateningly low blood pressure.

    06:31 So, this, angiotensin II, which my own body is capable of making with the RAAS, is 4-8 times as potent as norepinephrine.

    06:43 It's really impressive. That's why I told you it is a bad mama jama.

    06:47 So, the RAAS, the end products of that, end up with volume expansion and vasoconstriction.

    06:56 Now without looking at the screen, what I want you to do is to think through this diagram, see if you can look in the margin of your notes and recreate this diagram without looking at the notes.

    07:15 Okay, now, let's pretend that we have unlimited resources and finances, and you and I are going to solve the problem of treating hypertension.

    07:25 Now, if we look at this process, like a flow chart -- so let's say this is how the RAAS works, right? We've got renin, angiotensinogen, angiotensin I, ACE, and angiotensin II.

    07:38 Okay, so what kind of drugs could I design, based on these steps-- how could I interrupt these steps or interfere with these steps, and so I don't make it all the way down to the action of angiotensin II? Now, there is a point I want to point out.

    07:55 Angiotensin II, we know it is a really intense concept, right? It's a really amazing what it can do in the body, but it doesn't really do anything unless angiotensin II has available angiotensin II receptors.

    08:09 So before I get that -- all that reaction that we get, you want to make sure that the angiotensin II can actually make it to an angiotensin II receptor.

    08:20 Now that was a really big clue.

    08:22 If we're in an escape room together, that would have been a really big clue, but let's walk through it.

    08:27 Because what would happen if we for say, used direct renin inhibitors? If we could make a drug that would inhibit renin? Well, look at that. If I have less renin, I'm going to end up with less angiotensin II, and I'm going to end up with less angiotensin I, right, because there won't be as much renin available to connect with the circulating angiotensinogen, therefore, I have less of every other product downstream.

    08:57 Okay, cool. So if I have less renin, I'm going to end up with less potent vasoconstriction and volume expansion, because there's just going to be less available.

    09:08 So that would be cool if we could come up with a drug that would do that.

    09:13 Now, what if I could come up with a drug that just made less ACE available, less angiotensin-converting enzyme? Well, I'd still have lots of renin, angiotensinogen would be there. I'd have angiotensin I, but -- ah, that's why I wouldn't have as much -- and -- because if I have less ACE, I have less things available to convert angiotensin I to angiotensin II.

    09:43 Bueno, that means I will be able to lower my patient's blood pressure.

    09:49 Okay, so we've talked about direct renin inhibitors, and we've talked about ACE inhibitors.

    09:55 So we've hit the inhibitors. Let's talk about the blockers, okay? So, we've got a choice of angiotensin II receptor blockers or aldosterone receptor antagonist, or blockers.

    10:08 Okay. So, if I could create a drug that was an angiotensin II receptor blocker, that means that that is a drug -- Remember, we've got unlimited resources and money.

    10:21 That's a drug that is so uniquely created that it will slide right into an angiotensin II receptor.

    10:29 And once that drug is on there, it blocks off that receptor.

    10:35 So let's walk back through our flow chart.

    10:37 If I've given my patient an angiotensin II receptor blocker, will I have renin? Yes. Okay, well, then will I have circulating angiotensinogen? Yes. Well, then will I have angiotensin I? Yes. But if I've given them an angiotensin II receptor blocker, will I have ACE? Yes. So, will I end up with angiotensin II? Yes, you will, but here's the deal.

    11:10 It'll be all dressed up and no place to go because why? Because you were smart enough to give your patient an angiotensin II receptor blocker.

    11:20 Well, look at this receptor down here. It's all filled up.

    11:23 So when your body squirts out those substances and angiotensin II becomes available, it can't connect to the receptor because you wisely gave your patient an angiotensin II receptor blocker.

    11:37 So, without that angiotensin II connecting to the receptor, you're not going to have the potent -- vasoconstriction or volume expansion.

    11:50 Now, we've got another blocker up there.

    11:51 You can see that we called it an antagonist.

    11:54 Remember, we use those terms interchangeably, "antagonist" and "blocker." So, an aldosterone receptor antagonist, the same thing as an aldosterone receptor blocker.

    12:06 So, if I have a med that's an aldosterone receptor antagonist, that means that that medication is uniquely created, that it will fit and block the aldosterone receptors.

    12:20 With the receptors not being available, because you gave the patient a medication, the body's not going to know to hang on to sodium, right? So you're not going to have that water that follows, so your blood pressure will be lower.

    12:32 So that's why understanding how the RAAS works before we ever talked about the drugs, really, can help you understand their mechanism of action.

    12:43 If we have less renin, we definitely have less angiotensin II.

    12:47 If we have less ACE, angiotensin- converting enzyme, we're definitely going to have less angiotensin II.

    12:54 If we have an ARB, an angiotensin II receptor blocker, we're going to have angiotensin II, but without its ability to connect to an angiotensin II receptor, we're not going to have that normal vasoconstriction or volume expansion.

    13:10 If we try a patient on an aldosterone receptor blocker, we're not going to have the body hanging on to more sodium with water following for the volume expansion.

    13:19 So understanding the RAAS is a really simple and straightforward way to look at 4 groups or categories of antihypertensive medications.


    About the Lecture

    The lecture Renin-Angiotensin-Aldosterone-System (RAAS) (Nursing) by Rhonda Lawes is from the course Cardiovascular Medications (Nursing).


    Included Quiz Questions

    1. Angiotensin I
    2. Angiotensin II
    3. Angiotensinogen I
    4. Angiotensinogen II
    1. Angiotensin II
    2. ACE II
    3. Angiotensinogen II
    4. Aldosterone II
    1. Vasoconstriction
    2. Volume expansion
    3. Vasodilation
    4. Volume constriction
    1. Increase blood pressure
    2. Detoxify the liver
    3. Balance angiotensin I
    4. Lower blood pressure
    1. Aldosterone
    2. Adrenaline
    3. Angiotensinogen
    4. Angiotensin II
    1. Norepinephrine
    2. Insulin
    3. Angiotensin I
    4. Angiotensinogen
    1. Direct renin inhibitor
    2. Angiotensin II receptor blocker
    3. Aldosterone receptor antagonist
    4. ACE inhibitor

    Author of lecture Renin-Angiotensin-Aldosterone-System (RAAS) (Nursing)

     Rhonda Lawes

    Rhonda Lawes


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    She's hilarious. I love her!
    By Thiviet N. on 05. May 2019 for Renin-Angiotensin-Aldosterone-System (RAAS) (Nursing)

    Rhonda makes Pharmacology easy to comprehend. Her explanations are clear and funny.