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Kaplan Qbank USMLE



Author5 Posts
  #1

in some cases increased renin secretion for increasing CO causes renal vasoconstriction like in CHF. But I have seen constriction in the renal vessels also promoting SECRETION of renin in other avenues of path, which seems odd to me. wouldnt this exacerbate the situation and decrease GFR. thanks

  #2

1. Constricited renal arteries cause renin release
2. RAA axis cause an elevated bp and CO
3. Elevated CO cause more blood flow to the kidneys
4. This causes reduction in Renin release, and a fall in bp

  #3

this is how I see it:
as you said RAA system will cause the production of angiotensin II.
well this is a very potent vasoconstrictor. initially both afferent and efferent arteriols will constrict as a response to the activity of Angio II. then the local prostaglandins in the vicinity of the afferent arteriols will revers the vasoconstriction to vasodilatation in the afferent arteriole. but the efferent arteriole will remain vasoconstricted.
the vasodilated afferent arteriole will cause increased GFR, whereas vasoconstricted efferent arteriole will cause an increase in reabsorption of water and solutes especially in the PCT. →increasing the volume of blood →increased cardiac output → increase the BP.

  #4

hey gooshipoh,
u are simply getting confused b/w the normal homeostatc mechanisms and abnormal ones.
CO of 5 L /min is required normally to keep in balance with the RAA activity.... and reduction in CO as in CHF (where there is venous pooling)
would stimulate RAA more and more.... tht's why this system gets exaggerated in CHF and not normally where CO is well maintained.

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  #5

ok thanks









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