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Old 03-19-2013
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Kidney Sympathetic Stimulation and Sodium Reabsorption!

Need help understanding mechanism whereby inc. SANS ---> cause in inc. Na reabsoption from Proximal Tubule
I thought it had something to do with inc. Sympathetic Activity results in afferent artery vasoconstriction greater than efferent: this causes:

decreased GFR
and decreaed RPF

so its difficult to say what happens to Filtration Fraction (because both are decreased).

I mention Filtration Fraction, because I know that when filtration fraction is increased (inc. GFR), then glomerolutubular feedback will result in more reabsoportion. but i'm not sure this mechanism is related at all to the inc. in Sympathetic activity.
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Old 03-19-2013
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SNS stimulates the release of renin from JG cells, activating the RAA pathway. Angiotensin II increases reabsorption of Na+ in the proximal tubules.
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Old 03-21-2013
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Quote:
Originally Posted by slowpoke View Post
SNS stimulates the release of renin from JG cells, activating the RAA pathway. Angiotensin II increases reabsorption of Na+ in the proximal tubules.
yes thats is the answer
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Old 03-22-2013
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Quote:
Originally Posted by slowpoke View Post
SNS stimulates the release of renin from JG cells, activating the RAA pathway. Angiotensin II increases reabsorption of Na+ in the proximal tubules.
Through the same Beta 1 receptor which is not only in the heart, but also in kidneys controlling the function that @slowpoke mentions.
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Old 11-06-2016
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Renal nerve stimulation ( sympathetic outflow to kidney) stimulates Renin release! Renin proteolytic enzyme stored in JG cells of kidney. Angiotensin is the most powerful vasoconstrictor known!
Sodium reabsorption in the distal convoluted tubule n collecting duct occurs under effect of aldosterone which is increased by angiotensin2 which depends on Renin.
(are there aldosterone sensitive receptors in PCT?...no, ryt?)
Renin causes a lot of long term harm to CHF patient even though it is trying to compensate for decreased cardiac output.
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