Renin Angiotensin Aldosterone System (RAAS) - MADE SUPER EASY
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- Опубліковано 8 вер 2024
- Renin Angiotensin Aldosterone System (RAAS) EXPLAINED - MADE EASY
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RAAS
What is RAAS
How does aldosterone work on the kidneys
Renal Physiology
ACE Inhibitors
Angiotensin II works on Vascular smooth muscles causing vasoconstriction therefor increasing TPR (i think this is what ur books is referring to as Afferent arteriole, which is correct). at the same time Angiotensin II also works MAINLY on Efferent arterioles via vasoconstriction, causing a decrease in Renal Plasma Flow "RPF" & an increase in Filtration Fraction "FF" which ultimately results in an increase in GFR.
Remember (FF= GFR/RPF).
I'm pretty sure this is correct
I hope this helped :)
I have been struggling with the RAAS and this video is brilliant, it has totally given me a better understanding.... thank you x
another medical student really appreciates this.
Thank you!! Clear and detailed, without over explaining. Thanks for mentioning a side note or two, to put things into perspective, without trying to cover 3 lectures in one. Great tutorial!
+Danielle No Leaf, You are very welcome. We're glad you found this video helpful. All the best to you
Even after 11 years still a effect video, thank you for teaching ❤❤❤❤
Thank you! I have a nursing exam tomorrow and this made it crystal clear for me!
wow, I couldn't understand the RAAS system in class and I been told by two different instructors that we will need to know this as a nurse and it will come back to haunt us, if you do not learn it now. Thank you for this video, for now I understand this system completely. You definitely made this easy to understand!
You sir are a scholar and a gentleman!
I appreciate the conciseness, yet through way in which you explained the often complicated system. Thanks.
Pathophysiology: the biologic basis for disease in adults and children 6th edition states that the afferent and efferent artioles constrict from angiotensin II. That would mean that net hydrostatic pressure would not increase and GFR would not decrease. GFR would actually decrease because of decreased RBF. the explanations (if you have this book) is on p1352-1354.
Other than that thanks so much for this video, it really helped me understand this subject. good job and looking foreward to more
Very nice revision for my physiology exam thanks!
WOW !! 100 % concept clearity
Thank you so much for this excellent video. You have a gift for teaching.
Diane Cabello You are very welcome. Glad it was helpful :)
u have really made it easy to understand the concept....thank you so much.
Thank you! This was fantastic...I'm no longer getting cross eyed from reading about it
^.^
Thank you so much! I'll be sure to share this video with my students. It's always difficult to convey how RAAS works so clearly
thank you so much great explanation much needed for my patho class!
Helped this nursing student!
Same!
You are a boss at teaching
Cortisol increases Alpha1 receptor on blood vessels, leading to Vasoconstriction (e.g. Efferent arterioles in the kidneys) which is is similar to what Angiotensin 2 does to Efferent arterioles, therefore leading to increase in GFR! :)
Water tends to follow Na+ but without vasopressin there will be low/no levels of aquaporins and water will not be able to follow in the distal tubule and collecting duct. Ang II increases levels of vasopressin which is something you may like to mention to make your statement a little more correct.
very clear and easy to understand.
I dont know whats the error in this, i found it pretty good. Thanks.
Thank you so much! I was really struggling to learn this from my pathophysiology book but now, following this, I will be able to explain this , thank you!
Loved the lecture! Could you maybe do a lecture incorporate RAAS for cardio pharmacology?
Great lecture , keep it up .please give us more videos.
Thank you very much. You made it very easy to understand. Thumb up.
easy to understand thanks for making this video!!
That was a great presentation. Very well explained short but detailed and very easy to understand. Thank you so much!
thank you so much your work is excellent, has helped me understand the system so thoroughly, only one comment would be that near the end when you discussed kalemia and blood pressure I was not certain as to whether you said hyper or hypo, may be define these words so we make no mistakes. keep up the brilliant work.
karen
Hi. He said hypokalemia. Potassium is being excreted from the body, so it's a net loss. Hence Hypo-. Hopefully that helps :)
Aldosterone works on Principal cells causing reabsorption of Na and water. That is how it rises blood pressure :)
Really helped will be waiting for more!!! Thanks!!!
Lemme clear ur concept! As Angiotensin 2 constricts the efferent arterioles it increases the FF and GFR for a moment, but after extra fluid is filtered to the bowman's space,it will increases hydrostatic pressure of the bowman's space so will opposes filtration,hence GFR and FF will come to normal after sometime. hope it helps :)
Thank you! You did an excellent job breaking it all down and explaining it well. Keep making videos!
+Ti Gr Thank you very much. Glad the video was helpful for you. You can visit our new website for more awesome videos --> freemedicalvideos.com/
Thank you! I will!
I appreciate this so much! This is the only way I actually understood this concept! :)
Good review overall! But.. you didnt mention how Angiotensin II goes into to the brain to stimulate vasopressin release AND cause thirst. These are also important ways in which RAAS causes increase in BP.
You did a great job on RAAS:)...keep it up
That was really well explained, thank you so much :) - Nursing student
Easy to understand. Thanks !
Thank you so much! Your videos were unbelievably helpful :)
Thank you for drawing this all out. You made it very easy to understand. Great job!
You sir are far too kind! thank you :)
very comprehensive! Really helpful, thanks :)
Really helpful, thanks.Waiting for more from you.
Best explanation!!! thank you so much
it's a very good video, but u didnt talk about the AgII receptors, that it acts on a receptor for vasodilatation, and another for vasoconstriction. thank you
I really like how the relevant A&P is referenced; great job :)
@ Nobody Special, I absolutely agree! Great job sir!
Hi this is simply superb
Well said, if possible please illuminate secondary hyperaldosteronism , especially mechanisms of renal artery stenosis.
Here is a video on Conn's syndrome vs Secondary Hyperaldosteronism: ua-cam.com/video/7btgrDHnR4s/v-deo.html
Thank you! Awesome lecture really helped me understanding this system.
Very Very Helpful. Thank You!
Aldosterone causes the re-uptake of Sodium (salt) into the bloodstream. Water follows salt.... So instead of excreting water as urine, it follows the sodium into the bloodstream, therefore increasing blood volume, and in turn this increases blood pressure.
I hop you will be making more I will be following Thanx again
Excellent job...thank you
Great job. Well done
Thank you for this video, clear and understandable explanation. This has been very helpful for me :)
Excellent! Thank you!
Great job! very helpful!
That was so great! Thank you for your help!
+Kristi Hill, You are welcome. We're glad you found this video tutorial helpful. Please check out our other videos and feel free to share them with others :)
Perfect Thank you.
Very helpful, thanks
thank you for your effort
You won my suscription. Thank U.
Thank you for this!
Great man! Gracias!
Thank you! yes made super easy to understand
Thank you! I enjoyed watching your video. Now, I know what is going on! :) x
Thank you so much 🖐️
very helpful, thank you!
Excellent! Love it!
super
it is so easy and useful
usually Na+ K+ ATP-ase pumps 3Na+ out and 2K+ in. So there will be less NA and a lot of K in the cell. And that makes cell to let Na+ in and K+ out from the other side. The cell is located between blood vessel and the tube.
No?
simply amazing thank you!
Well done
Great video!
Great video
Good job!
great and thanx for ur help
Excellent video!
thank you. this was very helpful!
This is amazing. I have a question though, how does an ACE inhibitor differ from a diuretic?
Thank you so much! it was great
So helpful
Very nice!
thank you bro. good stuff
You didn't explain how angiotensinogen is converted to angiotensin 1 in the liver. Also the triggers of this system. But overall very thorough :)
Wow, awesome!
Had class about this the whole week, and I didn't understand a sh#t. Then I watched this awesome video for just 10 minutes and I understood everything...o.O. Thanx so MUCH and keep up the good work :D
Thanks for the video,, really helpful
Thanx that really helped
Thank You
There is a huge error in this video with regards to the Principal cell. When aldosterone acts on the Principal Cell, it causes the insertion of ENaC (Na+ reabsorbed) and ROMK (K+ secreted) channels. The video incorrectly describes this phenomenon as a sort of Na+/K+ exchanger which is not reality. It is also not an ATPase either which may mislead some students. Additionally, H20 simply does not follow Na+ and that's the end of the story. No, ADH is released into the blood during this situation and binds the V2 receptor on the anti-lumenal surface of the Principal cell. As a result, transcription and insertion of aquaporins on the lumenal surface occur; the aquaporins are endocytosed to allow a channel for H20 to pass through as Na+ is being absorbed into the Principal cell (and K+ is simultaneously being secreted).
brilliant! Thank you for this :)
Awesome!
thanks bud, really helped
+CMM Review, You are very welcome. We're glad you found our video tutorial helpful. Please feel free to share it with others :)
good video thanks
that was amazing. thank you!
Thanks sir
Wow, great review for me! Thank you!