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Old 09-02-2011
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Kidney Effects of Angiotensin II on GFR, RPF, and FF

A scientist seeks to evaluate the role of angiotensin II in changing GFR, RPF and FF. In the presence of angiotensin II, how will these measurements change?
A. GFR decreases, RPF increase, FF normal
B. GFR decrease, RPF no change, FF decrease
C. GFR decrease, RPF decrease, FF normal
D. GFR increase, RPF decrease, FF increase
E. GFR normal, RPF normal, FF increase
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D.

Angiotensin II constricts efferent arteriole so that less blood enters the glomerulus while pressure raises, leading to elevated GFR. Thus, FF is elevated too.
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Old 09-02-2011
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D. GFR increase, RPF decrease, FF increase

Angiotensin constricts efferent arterioles leading to inc GFR and dec RPF. FF=GFR/RPF, so FF inc.
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Old 09-02-2011
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D. GFR increase, RPF decrease, FF increase

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Old 09-02-2011
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(Answer: C)
AT-II --> constructs both renal efferent and efferent arteriolar but Efferent > Afferent --> renal resistance increase --> Renal plasma flow decrease And so the GFR decrease (not a big change though)
As FF= GFR/RPF and as both decrease, it seems reasonable that the FF will remain normal
so (GFR decrease, RPF decrease, FF normal)
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Old 09-02-2011
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D.RPF decrease ,GFR increase FF Increase
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Old 09-03-2011
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Inc GFR, Dec RPF and inc FF!
also FF=Gfr/RPF
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Old 09-03-2011
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agree with d
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Old 09-03-2011
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DDDDDDDDDDD
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Old 09-04-2011
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The correct answer is D.
The powerful vasoconstrictor angiotensin II preferentially constricts efferent arterioles. This constriction will increase GFR but will decrease RPF. Since FF = GFR/RPF, FF will also increase. Patients taking ACE inhibitors or angiotensin II receptor blockers will abolish this effect and will have a decreased GFR.
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Old 09-04-2011
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Quote:
Originally Posted by ricko335 View Post
The correct answer is D.
The powerful vasoconstrictor angiotensin II preferentially constricts efferent arterioles. This constriction will increase GFR but will decrease RPF. Since FF = GFR/RPF, FF will also increase. Patients taking ACE inhibitors or angiotensin II receptor blockers will abolish this effect and will have a decreased GFR.
I beg your pardon but please check the Kaplan physiology book and video on that subject and u will find the answer is C

Last edited by alaahoda2001; 09-04-2011 at 03:35 PM.
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Old 09-04-2011
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Quote:
Originally Posted by alaahoda2001 View Post
I beg your pardon but please check the Kaplan physiology book and video on that subject and u will find the answer is C
this may help:

Effects of Angiotensin II on GFR, RPF, and FF-aa-y-ae-glomerulo.png
click image to enlarge
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Old 09-05-2011
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Quote:
Originally Posted by bebix View Post
this may help:
Quote:
Originally Posted by bebix View Post
hey i think that we r dilating efferent only in picture c and dilating afferent in d.. am i right?
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Old 09-05-2011
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I have to say that before studying the Kaplan USMLE physiology course I was confused about the physiological effects of AT-II on the renal Afferent and efferent arteriolar, and I tended to go with answer D at that time. hover, after studying it I understood the following

Again, the effect of AT-II is not only on the efferent arteriole but rather on the both Afferent and efferent, and the fact that efferent > Afferent doesnot underestimate that AT-II increasing the resistance to flow inside the kidney and that decreases both flow and pressure and the efeerent constricts as much as it can in this case but it can only take the filtration pressure only close to normal with a net little decrese in the pressure --> minimal decreased GFR
On the other hand, when u use ACEI --> the exact opposie occur and that is why it is Contra-indicated in case of Renal artery stenosis (I can explain this later)

I have to say also that Unfortunately your reasoning has 2 weak points
1- in the question here It is not mentioned that the scientist will study the effect of AT-II in a case of pathologically increased levels, but rather in physiological situations (so no need to expect low vascular volume status)
2- AT-II does not actually increase COP because it causes increasing peripheral vascular resistance together with increasing pressure (CO=MAP/PVR)

Finally, I will later upload the part of the Kaplan nook and video in which it is mentioned that AT-II causes slight decrease in GFR
best wishes.

Last edited by alaahoda2001; 09-05-2011 at 01:36 AM.
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Old 09-05-2011
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Quote:
Originally Posted by bebix View Post
this may help:

Attachment 1903
hey BIBEX,
This is a Very good illustration that helps in understanding most situations
It really helped
Unfortunately, howver, the case of AT-II is not shown in this illustration, which is composed of Afferent constriction and efferent constriction but efferent > Afferent
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Old 09-09-2011
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A must know concept for usmle!

Know it well and It'll get you many answers right!
Also know what happens with urethral constriction, renal stenosis and stuff
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  #17  
Old 09-09-2011
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Quote:
Originally Posted by alaahoda2001 View Post
hey BIBEX,
This is a Very good illustration that helps in understanding most situations
It really helped
Unfortunately, howver, the case of AT-II is not shown in this illustration, which is composed of Afferent constriction and efferent constriction but efferent > Afferent
I know that AII will also Vc the AA, but since this effect is always greater in the AE...in the end you will have the same outcome (in both situations):

GRF up
RPF down
==> FF up
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Old 09-09-2011
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Quote:
Originally Posted by alaahoda2001 View Post
I have to say that before studying the Kaplan USMLE physiology course I was confused about the physiological effects of AT-II on the renal Afferent and efferent arteriolar, and I tended to go with answer D at that time. hover, after studying it I understood the following

Again, the effect of AT-II is not only on the efferent arteriole but rather on the both Afferent and efferent, and the fact that efferent > Afferent doesnot underestimate that AT-II increasing the resistance to flow inside the kidney and that decreases both flow and pressure and the efeerent constricts as much as it can in this case but it can only take the filtration pressure only close to normal with a net little decrese in the pressure --> minimal decreased GFR
On the other hand, when u use ACEI --> the exact opposie occur and that is why it is Contra-indicated in case of Renal artery stenosis (I can explain this later)

I have to say also that Unfortunately your reasoning has 2 weak points
1- in the question here It is not mentioned that the scientist will study the effect of AT-II in a case of pathologically increased levels, but rather in physiological situations (so no need to expect low vascular volume status)
2- AT-II does not actually increase COP because it causes increasing peripheral vascular resistance together with increasing pressure (CO=MAP/PVR)

Finally, I will later upload the part of the Kaplan nook and video in which it is mentioned that AT-II causes slight decrease in GFR
best wishes.
Just think in numbers here:

If Q = RPF = 600 ml/min
FF = GRF / RPF

Normal FF = 20% ==> GFR 120 / RPF 600

Vc (AA or EA) will decrease Q = new Q 400 (doesn't matter really the number here)

Since AII Vc EA >>>AA = Hydrostatic pressure between both arterioles will also increase => GFR increases (because this number depends on the hydrostatic and oncotic pressure, and since HP goes up => more filtration)

net outcome => FF > 20%

Remember, FF is a percentage of RPF and not an absolute value...so even if the GFR stays the same, since the denominator decreases, the percentage must increase!

good luck!

For more info, check here:
Concepts in medical physiology
http://books.google.com/books?id=A8H...action&f=false
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Old 09-09-2011
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First of all I chose C, cuz I had similar question in UW not long ago, but there was a case with the consticted renal artery in an experimental animal model (concieder this one as an afferent constriction - dec GFR, dec RPF, normal FF)
But then read one more time and realized that the answer is D.
Renin is released by juxtamedulary cells of the kidney in response to decreased Na... so, logically to increase the delivery of Na to Juxtamedullary cells renin is released and converted to Angiotesin and then to Angiotensin 2 to constrict (mainly efferent arteriole) and all other arterioles too, but efferent especially, so GFR will increase, RPF will go down and FF will increase.

Thats what I think
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Old 09-09-2011
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Quote:
Originally Posted by bebix View Post
Just think in numbers here:

If Q = RPF = 600 ml/min
FF = GRF / RPF

Normal FF = 20% ==> GFR 120 / RPF 600

Vc (AA or EA) will decrease Q = new Q 400 (doesn't matter really the number here)

Since AII Vc EA >>>AA = Hydrostatic pressure between both arterioles will also increase => GFR increases (because this number depends on the hydrostatic and oncotic pressure, and since HP goes up => more filtration)

net outcome => FF > 20%

Remember, FF is a percentage of RPF and not an absolute value...so even if the GFR stays the same, since the denominator decreases, the percentage must increase!

good luck!

For more info, check here:
Concepts in medical physiology
http://books.google.com/books?id=A8H...action&f=false
Well said Bibex,
i actually tend to say that answer D and that was my answr before i read the kaplan text and videos of 2010
please watch the video in the link below and tell me if you can explain it
i really want to know what do you think?


i
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Old 09-10-2011
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@alaahoda2001

Hi,

So, here we have the effect of AII: "preserve GFR & RPF decreases"

Then,
if FF = GFR / RPF and the normal values are FF = 120 / 600

FF = same GFR / decrease RPF
FF = 120 / 500

FF will increase
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Old 09-10-2011
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Quote:
Originally Posted by bebix View Post
@alaahoda2001

Hi,

So, here we have the effect of AII: "preserve GFR & RPF decreases"

Then,
if FF = GFR / RPF and the normal values are FF = 120 / 600

FF = same GFR / decrease RPF
FF = 120 / 500

FF will increase
Well, I have to admit that I am a bit confused now
Does this mean I should stop trusting Kaplan or what?

I want to add something,
Before explaining different factors affecting the GFR, the lecturer stressed on that factors affecting GFR do not strictly follow the mathematical equation of FF=GFR/RPF and we have to take Care of that and to study each situation separately (I will upload this video later too)
In my search on the internet too, I found a similar debate on the following link
http://www.prep4usmle.com/forum/thread/88674/
They said (and that goes with my opinion) that AT-II increases the GFR but not ba k to normal and that leads to a general effect of a minimal decrease of GFR
What do u think?
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  #23  
Old 09-10-2011
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@alaahoda2001

You should still trust Kaplan...hahaha...

I saw the video that you uploaded (kaplan) and if you read the slide, says "preserve GFR & RPF decreases" .... so, if you plug this on the equation you'll have a increase in FF (again, here the right answer would be D)

Now, this is from Guyton p 322

"Angiotensin II Constricts Efferent Arterioles. A powerful renal vasoconstrictor, angiotensin II, can be considered a circulating hormone as well as a locally produced autacoid because it is formed in the kidneys as well as in the systemic circulation. Because angiotensin II preferentially constricts efferent arterioles, increased angiotensin II levels raise glomerular hydrostatic pressure while reducing renal blood flow.
It should be kept in mind that increased angiotensin II formation usually occurs in circumstances associated with decreased arterial pressure or volume depletion, which tend to decrease GFR. In these circumstances, the increased level of angiotensin II, by constricting efferent arterioles, helps prevent decreases in glomerular hydrostatic pressure and GFR; at the same time, though, the reduction in renal blood flow caused by efferent arteriolar constriction contributes to decreased flow through the peritubular capillaries, which in turn increases reabsorption of sodium and water, as discussed in Chapter 27.
Thus, increased angiotensin II levels that occur with a low-sodium diet or volume depletion help preserve GFR and maintain normal excretion of metabolic waste products such as urea and creatinine that depend on glomerular filtration for their excretion; at the same time, the angiotensin II–induced constriction of efferent arterioles increases tubular reabsorption of sodium and water, which helps restore blood volume and blood pressure. This effect of angiotensin II in helping to “autoregulate” GFR is discussed in more
detail later in this chapter."

If you have time, take NBME 7 online!....
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  #24  
Old 03-31-2012
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Guys, if you check brs the correct answer is D but in kaplan it will be C, logically it's should be D.. I AM CONFUSED WITH THIS.
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  #25  
Old 09-30-2015
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Default Angiotensin II increases FF

I know you guys posted this info years ago, but for you or anyone who might still be interested in the answer. It's in definitively D.

The logic that you guys used to figure out that the slight decrease (according to Kaplan) in GFR causes an increase in FF has been scientifically observed and proven through research. Here is the article link (which also links to source research that contains the information).

http://pharmrev.aspetjournals.org/content/59/3/251.full

"The observation that Ang II increases the filtration fraction..."

Thank you to everyone above for sharing your knowledge!
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  #26  
Old 03-11-2016
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D. they are talking about constriction at the efferent arterioles.
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Old 03-14-2016
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D
AT II constricts the efferent --> HTN in the glomerulus --> increased hydrostatic pressure --> Increased GFR
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