new_n_lost
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Angiotensin 2 => constrict the efferent arterioles => inc GFR
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| babydoc4usmle
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agree with new-n-lost
with one correction
ATII constrict afferent & efferent arterioles, but efferent more, that is why we have increase in GFR
so, what are your points? seems to me it should be something interesting
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| Luckyall
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agree A 11 constricts both afferent&efferent, but more effect on Efferent
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| sany
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Hello friends
Thank you for your prompt rely.I raised this point because I have encounterd different views.Please follow me.
1.I fully understand that angiotensin 2 preferntially constricts the efferent arteriole and results in an increase of GFR.This clearly is mentioned in First aid.,step 1 2006.page page 378 & 381.Besides that part of the reason for the development of ACE inhibitors is this phenomena..(at times an advantage of decreasing GFR as in Diabetics with Hyperfiltration).
2.In Ganong..Angiotensons 2's stong vasoconstrictor effect is overempahsized like Norepinephrine ...causing afferent arteriolar constriction (no mention about efferent arteriole) and resulting in decrease GFR.
3.High yield histology 2004..page 184 and 185..says affects afferent and efferent arteriole and causes a decrease in GFR...period!
4.I have come across another point which says ..preferentially constricts efferent arterile at low doses!!..
So you know.,I think I have enough reason to bring this case to the attention of this forum so that we can come up with a reasonable conclusion...
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sany
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| sany
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Hello friends
Thank you for your prompt rely.I raised this point because I have encounterd different views.Please follow me.
1.I fully understand that angiotensin 2 preferntially constricts the efferent arteriole and results in an increase of GFR.This clearly is mentioned in First aid.,step 1 2006.page page 378 & 381.Besides that part of the reason for the development of ACE inhibitors is this phenomena..(at times an advantage of decreasing GFR as in Diabetics with Hyperfiltration).
2.In Ganong..Angiotensons 2's stong vasoconstrictor effect is overempahsized like Norepinephrine ...causing afferent arteriolar constriction (no mention about efferent arteriole) and resulting in decrease GFR.
3.High yield histology 2004..page 184 and 185..says affects afferent and efferent arteriole and causes a decrease in GFR...period!
4.I have come across another point which says ..preferentially constricts efferent arterile at low doses!!..
So you know.,I think I have enough reason to bring this case to the attention of this forum so that we can come up with a reasonable conclusion...
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sany
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| Ancylostoma
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what my experience is that it constricts afferents and efferent. But constricts the efferents more and thus there will be a decrease in renal plasma flow but no change or a very minimal change in GFR. I only studied physio from kaplan but I remember a graph or a paragraph in the kaplan notes about this change. sany this is the exact reason I dont really like first aid physio
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| sany
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Thank you for involving yourself on this discussion.I have also red Kaplan and like their serial lecture Notes...but this is really a big point which needs clarification.You know.,I didn't come across any confusing point of concept in First Aid so far.(just not to mention the issue of astrocytoma and meduloblastoma as of concept matter).
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sany
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| paganini
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Let's continue with this concept but deeper. A friend calls you and ask for medication to his father because he is now hypertensive, You indicate an ACE inhibitor, after using the drug the patient goes into acute renal failure (all labs say high creatinine and bun, etc) what happened?
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| new_n_lost
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Sany......... I have a Ganong 22 ed. pg 704 its is written abt Angiotensin II that it does constrict Efferent more than Afferent . n the same thing u mentioned in point 4 but its in Low Perfusion Pressure on the next pg under Autoregulation of RBF.
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| sany
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Hello Paganini;
I am aware of this fact...There is a calculated risk of renal failure with use of ACE inhibitors.But it is not overemphasized and is said to be reversible even with renal artery stenosis.(Lipincott's Pharmacolgy 2000 page 187.Concerning the information from Ganong .,I don't have the book on my shelf now.,but as discussion progesses I have to be able to give year of publication and page.
Thank you
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| Ancylostoma
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reading med essentials it looks like it says that incases of decrease blood flow to the kidney , there is decreased gfr. The decreased gfr causes decrease NA load and realease og angiotensin two. For some reason it says that the reflex will cause a dilation of afferent arteriole (macula densa cell derived?) and a constriction of the efferent (ag2 derived).
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| new_n_lost
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Here is a article which does mention on the effects of ACEI's on GFR n concomittant Renal Faliure. they have also mentioned the normal mechanism of A II
"The mechanism of the renin-angiotensin system in regulation of renal function is believed primarily to be due to the effect of angiotensin II on the efferent arteriolar tone keeping the pressure relatively constant in the glomerulus and thereby keeping GFR constant over a wide range of perfusion pressures, i.e. systemic BP."
http://www.pubmedcentral.nih.gov/botrender.fcgi?b...
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| sany
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hello new .,
you have brought a good material of 2001 which will put more light to the discussion as it does not support decrease or increase of GFR.
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sany
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| new_n_lost
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Did u read the whole article buddy i think the paragraph i have quoted from the article tells us enuf abt the effects of AII in maintainence of GFR.
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| sany
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Yes I did.
Thank you
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sany
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| sany
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You know I was curious and went to the text again ,I could not find still a clear statement on the relation between ACE inhibitors and GFR!! The fear of use is still there with bilateral renal aretry stenosis.Their paper (case report) is also not focusing on ACE inhibitors but angiotensin receptor antagonists where there is some difference in action mechanism too. Did I get you?? Probably something different since thier report?
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| new_n_lost
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i thought we were looking for the relationship of A II & GFR
now if u r looking for something else then sure tell us maybe we will also learn something new in the process thats whts discussion is abt isnt it
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FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."
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| sany
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Hi new...No! I will be happy if we can focus just on angiotensin 2 and GFR.I have not raised a question that I know the answer.You know.,my worry is .,I really don't know what to say if I am asked to chose between decrease and increase in the actual exam.However ,if you ask me what would my opinion be from the available fact so far ..then I can put my view like one of us in the forum. By the way I am in the last month of the test schedule.,unless I change it based on NBME 3 & 4 which I will be taking in the coming 3-4 days.
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sany
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| werther
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Folks, i strongly recommend reading Goodman and Gilman's when it comes to dynamics...
check this out:
Reductions in renal blood flow markedly attenuate renal excretory function, and angiotensin II reduces renal blood flow by directly constricting the renal vascular smooth muscle, by enhancing renal sympathetic tone (a CNS effect), and by facilitating renal adrenergic transmission (an intrarenal effect). Angiotensin II–induced vasoconstriction of preglomerular microvessels is enhanced by endogenous adenosine owing to an interaction between the signal-transduction systems activated by AT1 and the adenosine A1 receptors (Hansen et al., 2003). Autoradiographic and in situ hybridization studies indicate a high concentration of AT1 receptors in the vasa recta of the renal medulla, and angiotensin II may reduce Na+ excretion in part by diminishing medullary blood flow. Angiotensin II variably influences glomerular filtration rate (GFR) via several mechanisms: (1) constriction of the afferent arterioles, which reduces intraglomerular pressure and tends to reduce GFR, (2) contraction of mesangial cells, which decreases the capillary surface area within the glomerulus available for filtration and also tends to decrease GFR, and (3) constriction of efferent arterioles, which increases intraglomerular pressure and tends to increase GFR. The outcome of these opposing effects on GFR depends on the physiological state. Normally, GFR is slightly reduced by angiotensin II; however, during renal artery hypotension, the effects of angiotensin II on the efferent arteriole predominate so that angiotensin II increases GFR. Thus blockade of the renin–angiotensin system may cause acute renal failure in patients with bilateral renal artery stenosis or in patients with unilateral stenosis who have only a single kidney.
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| sany
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Thank you werther for your explanation from Goodman & Gilman.As I have mentioned earlier the following is an information from Ganong.
Review of Medical Physiology 21st edition Lange ..Ganong chapter24 ,page 460....I hope ...new.. will be interested to see the detail..
Actions of angiotensins.........additional actions of angiotensin 2 include facilitation of release of norepinephrine by a direct action on the post ganglionic sympathetic neurons, contraction of the mesangial cells with resultant decrease in GFR and a direct effect on the renal tubles to increase sodium reabsorption.
I am presenting this desription.not because I liked the description but " new " wanted to know the source ,The main point ,in this statement is the decrease in GFR !!......From what we have discussed so far the point of werther is pointing to a conclusive remark but we can keep on exchanging ideas.
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sany
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| new_n_lost
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werther wrote:
Folks, i strongly recommend reading Goodman and Gilman's when it comes to dynamics...
check this out:
Reductions in renal blood flow markedly attenuate renal excretory function, and angiotensin II reduces renal blood flow by directly constricting the renal vascular smooth muscle, by enhancing renal sympathetic tone (a CNS effect), and by facilitating renal adrenergic transmission (an intrarenal effect). Angiotensin II��"induced vasoconstriction of preglomerular microvessels is enhanced by endogenous adenosine owing to an interaction between the signal-transduction systems activated by AT1 and the adenosine A1 receptors (Hansen et al., 2003). Autoradiographic and in situ hybridization studies indicate a high concentration of AT1 receptors in the vasa recta of the renal medulla, and angiotensin II may reduce Na+ excretion in part by diminishing medullary blood flow. Angiotensin II variably influences glomerular filtration rate (GFR) via several mechanisms: (1) constriction of the afferent arterioles, which reduces intraglomerular pressure and tends to reduce GFR, (2) contraction of mesangial cells, which decreases the capillary surface area within the glomerulus available for filtration and also tends to decrease GFR, and (3) constriction of efferent arterioles, which increases intraglomerular pressure and tends to increase GFR. The outcome of these opposing effects on GFR depends on the physiological state. Normally, GFR is slightly reduced by angiotensin II; however, during renal artery hypotension, the effects of angiotensin II on the efferent arteriole predominate so that angiotensin II increases GFR. Thus blockade of the renin��"angiotensin system may cause acute renal failure in patients with bilateral renal artery stenosis or in patients with unilateral stenosis who have only a single kidney.
The Reason i said Inc in GFR was due to its Effect on Efferent if something is Constricting the Efferent Arterioles the net resultant effect will be Inc GFR.
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| epica
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Inc in GFR was due to its Effect on Efferent agree
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