Renal perfusion

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studylol

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Hello friends,

I got a question wrong and i'm trying to figure out how afferent and efferent arterioles change their sm. muscle tone during hypovolemia.

What I do know: During hypovolemia, both afferent and efferent arterioles constrict.

What I want to know: How does it get there?

One question in particular: I know angII causes efferent constriction preferentially over afferent. FA says that JG cells (in the afferent arteriole) maintains GFR via RAAS. How do I reconcile these two facts?

Thanks!

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Update: UWORLD says that both afferent and efferent constrict. FA writes about efferent only (doesn't disagree, just doesn't describe afferent). I give up trying to understand UWORLD and i'm going the following. In case it helps anybody:

In response to hypotension, JG cells release renin --> AngII. AngII cause constriction of the efferent arterioles. Efferent constriction reduces renal perfusion rate but elevate filtration fraction. The net effect of this is to reduce blood going into the kidneys but maintain filtration/urine production during hypovolemic states. Although, less urine is produced due to aldosterone. But it's still being made.
 
I think from what I remember that both afferent and efferent constrict, but efferent constricts more- this increasing the hydrostatic pressure in the capillaries of Bowmans capsule, which increases GFR. Am I understanding this correctly?
 
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I think from what I remember that both affwrent and efferent constrict, but efferent constricts more- this increasing the hydrostatic pressure in the capillaries of Bowmans capsule, which increases GFR. Am I understanding this correctly?

Yes you are. What I have trouble understanding is what causes the afferent constriction and how that plays into the bigger picture.
 
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