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Old 06-02-2011
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Kidney Sympathetic stiumulation effect on kindney

Kaplan says effect of sympathetic stimulation on kidney is the following

decrease GFR
increase FF
increase forces promoting reabsorption

Can some one explain dominant effect of sympathetic stimulation is on afferent or efferent arteriole?? and plz mention detail

thanx
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Old 06-02-2011
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Sympathetic will primarily slow down, so by its action we know that it will cause constriction. (Sorry, I dont know if its afferent, or efferent), I think it was afferent.

By decreasing blood flow, you will decrease GFR, and thereby increase filtration fraction (dec. GFR/dec. RPF). Also by slowing down blood flow, you have a increase in renal glomerular hydrostatic pressure, which will promote reabsorption.

Last edited by patelMD; 06-03-2011 at 01:24 AM.
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F.F = GFR/RPF

if we dec both GFR and RPF how F.F is increased it should be decreased too

secondly i think increased reabsorption is due to increased oncotic pressure in peritubular capillaries not due to increased glomerular hydrostaic presuure..

what u say of it?
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Old 06-03-2011
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Quote:
Originally Posted by IKR123 View Post
F.F = GFR/RPF

if we dec both GFR and RPF how F.F is increased it should be decreased too

secondly i think increased reabsorption is due to increased oncotic pressure in peritubular capillaries not due to increased glomerular hydrostaic presuure..

what u say of it?
Oncotic pressure is pressure from serum proteins, so I dont think proteins are filtered in the first place, so how could there be increased oncotic pressure?

sorry, only GFR is decreased, RPF is invariable because either afferent or efferent arteriole is constricted, never both.
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oncotic pressure is of proteins so during filteration no protein is filtered and more free fluid is filtered ......> leading to more protein conc in peritubular capillaries ----> increased oncotic pressure of PERITUBULAR capillaries--->leading to increased reabsorbtion..(increased hydrostatic pressure of glumerulas cant leaed to increased reabsorption..

BUT AS FAR AS AFFECT OF SYMPATHETIC STIMULATION IS CONCERNED I AM STILL CONFUSED ABOUT MECHANISM OF ACTION..either afferent or efferent.
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Quote:
Originally Posted by IKR123 View Post
oncotic pressure is of proteins so during filteration no protein is filtered and more free fluid is filtered ......> leading to more protein conc in peritubular capillaries ----> increased oncotic pressure of PERITUBULAR capillaries--->leading to increased reabsorbtion..(increased hydrostatic pressure of glumerulas cant leaed to increased reabsorption..

BUT AS FAR AS AFFECT OF SYMPATHETIC STIMULATION IS CONCERNED I AM STILL CONFUSED ABOUT MECHANISM OF ACTION..either afferent or efferent.
When afferent arterioles constrict, glomerular filtration pressure decreases and therefore less glomerular filtrate is formed. When less glomerular filtrate is formed, less urine is ultimately formed.

There was a picture that Mondoshawan posted some time ago, that explained it really well..
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Quote:
Originally Posted by patelMD View Post
When afferent arterioles constrict, glomerular filtration pressure decreases and therefore less glomerular filtrate is formed. When less glomerular filtrate is formed, less urine is ultimately formed.

There was a picture that Mondoshawan posted some time ago, that explained it really well..
plzz give me link of dat pic..as i am much confused bout this concept
thanks
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Old 06-03-2011
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Default Step 1 question

hi i had a Step 1 question just asking the mechanism of using Ace inhibitors--so of course just know they prevent constriction of efferent arterioles and thus dilate and decrease GFR to prevent overfiltration and furthur kidney damage. gluck.
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for reference plz see kaplan physiology 2011 edition page 200
thanx
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