Angiotension II - Effect on Renal Blood Flow ?

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Ludacris

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Just did a NBME 7 question with the anesthetized dog asking the effects of Angiotensin II.

Why is Renal Blood Flow not decreased after infusion of Angiotensin II?

I know the Filtration Fraction would increase (GFR/RPF)... because GFR increases and RPF decreases... But why wouldn't RBF decrease also?

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Just did a NBME 7 question with the anesthetized dog asking the effects of Angiotensin II.

Why is Renal Blood Flow not decreased after infusion of Angiotensin II?

I know the Filtration Fraction would increase (GFR/RPF)... because GFR increases and RPF decreases... But why wouldn't RBF decrease also?

it does. my understanding was RPF and RBF is almost the same.
 
Just did a NBME 7 question with the anesthetized dog asking the effects of Angiotensin II.

Why is Renal Blood Flow not decreased after infusion of Angiotensin II?

I know the Filtration Fraction would increase (GFR/RPF)... because GFR increases and RPF decreases... But why wouldn't RBF decrease also?

Angiotensin does decrease RBF , it constricts both arterioles (although it has better effect on the efferent), increases resistance and thereby decreasing blood flow.
 
Hmmm... so does that question have 2 answers?

One option is Increased FF and the other is Decreased RBF.

I can post the entire question but I'm not sure if it's allowed...
 
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Why did you say that GFR increases?

Because it does not ( or to be more accurate ... it depends)

As i wrote , since the efferent arteriole is more sensitive to angiotensin than the afferent ... Small amounts of angiotensin would constrict it (increasing GFR) because of this sensitivity.

Now , large amounts of angiotensin however constricts both arterioles , and thereby decrease GFR.
 
Why did you say that GFR increases?

Because it does not ( or to be more accurate ... it depends)

As i wrote , since the efferent arteriole is more sensitive to angiotensin than the afferent ... Small amounts of angiotensin would constrict it (increasing GFR) because of this sensitivity.

Now , large amounts of angiotensin however constricts both arterioles , and thereby decrease GFR.

While you're right that large amounts of angiotensin constrict both arterioles, I think you're missing the key of angiotensin/the RAAS system and what it does for the kidney. The whole point of the RAAS system is to increase GFR by constricting the efferent arteriole so that more sodium can be reabsorbed. What signals it? Low blood volume, which is detected by the macula densa cells in response to low sodium. It makes no sense for it to be stimulated just so that it can decrease GFR further.
 
Hmmm... so does that question have 2 answers?

One option is Increased FF and the other is Decreased RBF.

I can post the entire question but I'm not sure if it's allowed...

please just post the quetion with the answer choices, its not a big deal to post 1 NBME question, esp when you summarise it, seriously.
There are subtle changes in FF depending on the level of ATII.
 
Here's the question (it's the first one) and a related question that I was confused about. http://i.imgur.com/pyP5W.png

In the 2nd question, Angiotensin II would be increased due to the decreased BP, right? So is the answer increased GFR or increased K+ excretion (secondary to Aldosterone secretion by Ang II)?

Why can't NBME just give full answer explanations... especially after paying $50-60!
 
While you're right that large amounts of angiotensin constrict both arterioles, I think you're missing the key of angiotensin/the RAAS system and what it does for the kidney. The whole point of the RAAS system is to increase GFR by constricting the efferent arteriole so that more sodium can be reabsorbed. What signals it? Low blood volume, which is detected by the macula densa cells in response to low sodium. It makes no sense for it to be stimulated just so that it can decrease GFR further.

Nahh .... In your case decreased blood pressure activates RAAS ,right?
Then RAAS (angiotensin) constricts both arterioles (as i wrote) because you want to keep your blood pressure up so you sort of "sacrifice" the blood flow to the kidney.
The effect of angiotensin(RAAS) and the increased sympathetic activity leads to a decrease in GFR and RBF.

Angiotensin ,however, increases aldosterone ... and that's what increases the reabsorption of sodium in the tubules.

FF however increases a little (because i believe RBF decrease is greater than the decrease in GFR).

Are we on the same page here?
 
Ops i somehow answered that in my reply to Parietal Lobe....

Here is what i think :

Decreased RBF is more likely than increased FF.

And aldosterone cause increased K excretion.


Good Luck OP ! :xf:
 
Nahh .... In your case decreased blood pressure activates RAAS ,right?
Then RAAS (angiotensin) constricts both arterioles (as i wrote) because you want to keep your blood pressure up so you sort of "sacrifice" the blood flow to the kidney.
The effect of angiotensin(RAAS) and the increased sympathetic activity leads to a decrease in GFR and RBF.

Where are you getting your information? I ask because you're wrong. The RAAS system absolutely, 100% leads to an increase in GFR. Read First Aid, read BRS, read RR Path. All of those sources will explain it to you. Ang II --> vasoconstriction on the efferent arteriole of the kidney --> increased GFR --> increased volume --> (eventually) increased blood pressure.

Angiotensin ,however, increases aldosterone ... and that's what increases the reabsorption of sodium in the tubules.

How do you think aldosterone is increasing reabsorption of sodium in the tubules if GFR is decreased?

FF however increases a little (because i believe RBF decrease is greater than the decrease in GFR).

Even with your reasoning, that doesn't make sense. FF = GFR/RPF. If GFR is decreased, how is FF increased?

Are we on the same page here?

No, we're not. I think you're wrong.
 
Where are you getting your information? I ask because you're wrong. The RAAS system absolutely, 100% leads to an increase in GFR. Read First Aid, read BRS, read RR Path. All of those sources will explain it to you. Ang II --> vasoconstriction on the efferent arteriole of the kidney --> increased GFR --> increased volume --> (eventually) increased blood pressure.

someone seems to feel very strongly about this subject (joke). but in my opinion redcard is correct.
you do not increase GFR, you are merely maintaining it.
this is a bit more complex and not as simple as you outline. initially there is an increase in GFR and filtration fraction but there is an increase in oncotic pressure in the glomerular capillary (the opposite of choice D esp after 1 hr of ATII infusion). now this change reduces GFR, obviously not as much as prior to or the initial few minutes of ATII infusion.

but hey I've been wrong before.

and OP the second question is more clear on this. that guy has been in CCF for a while so the answer is not increased GFR, it is increased K+ excretion as pointed out by redcard.
 
While you're right that large amounts of angiotensin constrict both arterioles, I think you're missing the key of angiotensin/the RAAS system and what it does for the kidney. The whole point of the RAAS system is to increase GFR by constricting the efferent arteriole so that more sodium can be reabsorbed. What signals it? Low blood volume, which is detected by the macula densa cells in response to low sodium. It makes no sense for it to be stimulated just so that it can decrease GFR further.

1. again, the point is not to increase GFR but to maintain it.


2. the decrease is in comparison to normal GFR not the low GFR that initiated the RAAS.
 
someone seems to feel very strongly about this subject (joke). but in my opinion redcard is correct.
you do not increase GFR, you are merely maintaining it.

Maintaining it? GFR is low, which is why the Macula Densa cells get the whole process rolling. Why would you maintain low GFR?

But don't take my word for it.

First Aid 2011, page 464 -- "AT II -- synthesized in response to low BP; causes efferent arteriole constriction --> increased GFR, increased FF, but with compensatory Na reabsorption in proximal and distal nephron. Net effect: preservation of renal function in low volume state with simultaneous Na reabsorption decrease additional volume loss.

BRS Phys 4th Edition, page 156 -- "At low concentrations, Angiotensin II preferentially constricts efferent arterioles, thereby protecting (increasing) the GFR."

And the parenthesis with the word "increasing" is theirs, not mine.
 
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I don't understand this topic myself as I haven't done renal yet, but according to Costanzo (the big Costanzo, pg. 254, 4th Ed):


Low Level Ang-II ---> decreased RPF, and increased GFR


High Level Ang-II ---> decreased RPF, and a smaller decrease in GFR (i.e. smaller in comparison to the reduction in RPF)


In both scenarios, FF will increase. FF = GFR/RPF, so the first scenario is obvious since the numerator increases and the denominator decreases. In the second scenario the denominator has a larger decrease, so FF also increases. At least that is my understanding and a cursory search on Wikipedia seems to support this. I mean, increasing FF --> increased osmotic pressure in the peritubular caps, and increased reabsorption, no? That would make sense, i.e. in a hemorrhage situation. BTW, I don't want to look at the actual question since I haven't started studying for the step yet and I am only responding because it helps me to understand things by explaining them (especially if I don't understand the concept, lol)
 
Maintaining it? GFR is low, which is why the Macula Densa cells get the whole process rolling. Why would you maintain low GFR?

But don't take my word for it.

First Aid 2011, page 464 -- "AT II -- synthesized in response to low BP; causes efferent arteriole constriction --> increased GFR, increased FF, but with compensatory Na reabsorption in proximal and distal nephron. Net effect: preservation of renal function in low volume state with simultaneous Na reabsorption decrease additional volume loss.

BRS Phys 4th Edition, page 156 -- "At low concentrations, Angiotensin II preferentially constricts efferent arterioles, thereby protecting (increasing) the GFR."

And the parenthesis with the word "increasing" is theirs, not mine.

maybe I wasnt clear, I meant maintaining it in relation to normal GFR which is evidently an increase from where it is during low volume. you write increased GFR in the second question you will not get the mark because it is not an increase compared to normal GFR.
 
and OP the second question is more clear on this. that guy has been in CCF for a while so the answer is not increased GFR, it is increased K+ excretion as pointed out by redcard.

Nope. The EKG showed no abnormalities. If this had been going on for a while, like you say, and potassium excretion was taking place, he'd be hypokalemic and hypokalemia would lead to EKG abnormalities. The answer is increased GFR.
 
I don't understand this topic myself as I haven't done renal yet, but according to Costanzo (the big Costanzo, pg. 254, 4th Ed):


Low Level Ang-II ---> decreased RPF, and increased GFR


High Level Ang-II ---> decreased RPF, and a smaller decrease in GFR (i.e. smaller in comparison to the reduction in RPF)


In both scenarios, FF will increase. FF = GFR/RPF, so the first scenario is obvious since the numerator increases and the denominator decreases. In the second scenario the denominator has a larger decrease, so FF also increases. At least that is my understanding and a cursory search on Wikipedia seems to support this. I mean, increasing FF --> increased osmotic pressure in the peritubular caps, and increased reabsorption, no? That would make sense, i.e. in a hemorrhage situation. BTW, I don't want to look at the actual question since I haven't started studying for the step yet and I am only responding because it helps me to understand things by explaining them (especially if I don't understand the concept, lol)

nope. in the second case you have normal FF not increased.
 
Nope. The EKG showed no abnormalities. If this had been going on for a while, like you say, and potassium excretion was taking place, he'd be hypokalemic and hypokalemia would lead to EKG abnormalities. The answer is increased GFR.

for a while is a relative term. I meant a few hours.
and do you really think the normal RAAS causes hypokalemia which will show on ECG?
 
maybe I wasnt clear, I meant maintaining it in relation to normal GFR which is evidently an increase from where it is during low volume. you write increased GFR in the second question you will not get the mark because it is not an increase compared to normal GFR.

Who said anything about raising it higher than normal GFR? The point is, you're increasing GFR with Ang II, which goes against what Redcard said.

Nahh .... In your case decreased blood pressure activates RAAS ,right?
Then RAAS (angiotensin) constricts both arterioles
(as i wrote) because you want to keep your blood pressure up so you sort of "sacrifice" the blood flow to the kidney.
The effect of angiotensin(RAAS) and the increased sympathetic activity leads to a decrease in GFR and RBF.
 
Who said anything about raising it higher than normal GFR? The point is, you're increasing GFR with Ang II, which goes against what Redcard said.

yes, I mentioned that now a few times, initially you do but as you increase it the oncotic pressure in the glomerular capillary builds up as the efferent arteriole is constricted even more with increased amounts of ATII. this increases glomerular capillary oncotic pressure which outweighs or equals the hydrostatic pressure which was initially causing increased GFR.
 
nope. in the second case you have normal FF not increased.

From Wikipedia (not claiming Wiki is not always right, but FWIW)

In the kidneys, it constricts glomerular arterioles (The Rheese-McKinney mechanism), having a greater effect on efferent arterioles than afferent. As with most other capillary beds in the body, the constriction of afferent arterioles increases the arteriolar resistance, raising systemic arterial blood pressure and decreasing the blood flow. However, the kidneys must continue to filter enough blood despite this drop in blood flow, necessitating mechanisms to keep glomerular blood pressure up. To do this, angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. The glomerular filtration rate (GFR) is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow. Because the filtration fraction has increased, there is less plasma fluid in the downstream peritubular capillaries. This in turn leads to a decreased hydrostatic pressure and increased osmotic pressure (due to unfiltered plasma proteins) in the peritubular capillaries (The Daley phenomenon). The effect of decreased hydrostatic pressure and increased osmotic pressure in the peritubular capillaries will facilitate increased reabsorption of tubular fluid.
 
I'm even more confused now 🙁 lol ...I'm going to read through this carefully in a bit and try to understand it.
 
Zenfudge, wiki ignores levels of ATII.
look, by your reasoning choice A(Increased filtration fraction) and choice E(Decreased Renal Blood Flow) would both be valid at the same time, Im sure we can agree that the NBMEs arent that stupid.
 
yes, I mentioned that now a few times, initially you do but as you increase it the oncotic pressure in the glomerular capillary builds up as the efferent arteriole is constricted even more with increased amounts of ATII. this increases glomerular capillary oncotic pressure which outweighs or equals the hydrostatic pressure which was initially causing increased GFR.

You're taking a question and turning it into more than it asks, in my opinion. The question is about an Ang infusion over 60 minutes. What results? Both decreased RBF and increased FF result. The other thing that results (which wasn't an answer choice) is increased GFR.

As for the second question, yes, I do agree that potassium excretion is a possible right answer, depending on how long this has been going on (because like I said, there were no changes on the EKG and there would have been with K excretion).

When I started this back-and-forth, it was in response to Redcard's claim that Ang II doesn't cause an increase in GFR. I wasn't addressing a specific question.
 
You're taking a question and turning it into more than it asks, in my opinion. The question is about an Ang infusion over 60 minutes. What results? Both decreased RBF and increased FF result. The other thing that results (which wasn't an answer choice) is increased GFR.

As for the second question, yes, I do agree that potassium excretion is a possible right answer, depending on how long this has been going on (because like I said, there were no changes on the EKG and there would have been with K excretion).

When I started this back-and-forth, it was in response to Redcard's claim that Ang II doesn't cause an increase in GFR. I wasn't addressing a specific question.

not in agreement with that NBME7 question, why dont you look for yourself?
 
Zenfudge, wiki ignores levels of ATII.
look, by your reasoning choice A(Increased filtration fraction) and choice E(Decreased Renal Blood Flow) would both be valid at the same time.

Which is the OP's original point. What do you suggest is the right answer to question 1?
 
Zenfudge, wiki ignores levels of ATII.
look, by your reasoning choice A(Increased filtration fraction) and choice E(Decreased Renal Blood Flow) would both be valid at the same time, Im sure we can agree that the NBMEs arent that stupid.



Yeah, you're right it does ignore the levels, just realized that. I still don't see how FF is not increased mathematically (in either scenario), given the explanation in Costanzo.
 
I thought you were not looking at the question which would have included 2 right answers which we can agree can not be the case.

I was looking at the question and I still say there are two right answers. It's either an error or there isn't enough information there to give us a clue as to what they're going for.
 
I was looking at the question and I still say there are two right answers. It's either an error or there isn't enough information there to give us a clue as to what they're going for.

seriously? you are going for "the idiots at the NBMEs made a mistake"?
as Zenfudge pointed out, in either case choice E would be correct.
 
seriously? you are going for "the idiots at the NBMEs made a mistake"?
as Zenfudge pointed out, in either case choice E would be correct.

You're the only person in this thread who's called them idiots. No one else has. If you think it's impossible for the NBME to make a mistake, I feel sorry for you.
 
Whooops what just happened here good people !?

Now that thing is a bit tricky and it all depends on how your book interpret the angiotensin action on both arterioles .

When i replied earlier i was basing it on costanzo(big costanzo) and my understanding of guyton.

Now Costanzo (Big Costanzo) says clearly that angio. constricts both arterioles + sympathetic activity which decreases GFR and RBF. (like zenfudge i think already quoted)

Guyton ,however, takes a more diplomatic approach saying that angio. trys to maintain GFR close to normal (and since in most of cases GFR is already decreased ... trying to maintain it would be like an increase in relation to the already decreased state ) and i don't remember whether guyton took into account the amount of angio. being given.

Now FA and BRS don't seem to care much about the afferent arteriole and so the constriction is only on efferent thereby GFR would increase. (BRS says however that it all depends on amount of angio.)

I doubt that the question is wrong since it is obviously there since 2009. ( or what do i know ? it might be ).

Poor OP for getting even more confused.

I still believe what i wrote earlier (which was based on Costanzo and my understanding of Guyton) :

decreased blood pressure activates RAAS ,right?
Then RAAS (angiotensin) constricts both arterioles (as i wrote) because you want to keep your blood pressure up so you sort of "sacrifice" the blood flow to the kidney.
The effect of angiotensin(RAAS) and the increased sympathetic activity leads to a decrease in GFR and RBF.


FF however increases a little (because i believe RBF decrease is greater than the decrease in GFR). ""Or even if one would consider the GFR maintained not decreased ""

Ops i somehow answered that in my reply to Parietal Lobe....

Here is what i think :

Decreased RBF is more likely than increased FF.

And aldosterone cause increased K excretion.


Good Luck OP ! :xf:

now i bolded the answer of the first question too because it's true both choices can be right , however maintaining normal blood pressure is essential .....So the body has to decrease the blood supply to the kidney thereby decreasing GFR which is way more important than the little increase in FF.

Plus that FF might not increase after all if GFR decrease is the same as RBF decrease.
 
Whooops what just happened here good people !?

Now that thing is a bit tricky and it all depends on how your book interpret the angiotensin action on both arterioles .

When i replied earlier i was basing it on costanzo(big costanzo) and my understanding of guyton.

Now Costanzo (Big Costanzo) says clearly that angio. constricts both arterioles + sympathetic activity which decreases GFR and RBF. (like zenfudge i think already quoted)

Guyton ,however, takes a more diplomatic approach saying that angio. trys to maintain GFR close to normal (and since in most of cases GFR is already decreased ... trying to maintain it would be like an increase in relation to the already decreased state ) and i don't remember whether guyton took into account the amount of angio. being given.

Now FA and BRS don't seem to care much about the afferent arteriole and so the constriction is only on efferent thereby GFR would increase. (BRS says however that it all depends on amount of angio.)

I doubt that the question is wrong since it is obviously there since 2009. ( or what do i know ? it might be ).

Poor OP for getting even more confused.

I still believe what i wrote earlier (which was based on Costanzo and my understanding of Guyton) :





now i bolded the answer of the first question too because it's true both choices can be right , however maintaining normal blood pressure is essential .....So the body has to decrease the blood supply to the kidney thereby decreasing GFR which is way more important than the little increase in FF.

Plus that FF might not increase after all if GFR decrease is the same as RBF decrease.

Decreasing RBF is the wrong answer for that question.
 
So I created a username for the sole purpose of resurrecting this thread and answering the OP's question as I too was miffed at this question and couldn't figure it out as to why there seems to be two correct answers. I found other threads online covering this same question with no definitive solution.

Then it dawned on me (After I remember being burned by a similar question in mammalian physiology undergrad classes) , the answer lies in the stem of the question as usual.

I think this thread has established the fact that administering pure Angiotensin II will both increase the filtration fraction and decrease renal blood flow with relatively equal degrees of certitude. However, the question stem poses that an INTRAVENOUS INFUSION is administered to the dog. That implies that there is a substantial amount of infusion volume (presumably saline) that is added to the dog's circulation system which could logically and paradoxically INCREASE renal blood flow or at least mitigate the effect of Angiotensin II decreasing renal blood flow. Because the saline administered with the Angiotensin II has no effect on the vasoconstrictive properties of Angiotensin II, it stands to reason that Angiotensin II's effect of increasing filtration fraction will not be affected by the presence of the infusion saline. Therefore the answer is unequivocally "increased filtration fraction" and not "decreased renal blood flow."

I got this question wrong as well. They haven't changed it since the OP posted. Sorry to resurrect this thread, but I did it to help out any others that may be stumped by the same question.
 
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