NBME 13 Renin angiotensin aldosterone concept help!

Discussion in 'Step I' started by abelabbot, 05.19.14.

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  1. abelabbot

    abelabbot Banned Banned Account on Hold 2+ Year Member

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    1) Someone clear this up for me. Renin is released in response to a decrease in blood pressure, decreased sodium delivery to distal tubule, and due to increased sympathetic tone?So when patients have hypertension, there is increased blood pressure, however renin STILL gets released..Why the heck is that? does this have to do with the fact that "renin is released also due to increased sympathetic tone"? If anyone has a simple way of understanding this, please do share. I thought I knew enough about this subject to get uworld questions right but nbmes showed me I don't have a mastery of this concept.

    2) Okay so the early DISTAL CONVOLUTED TUBULE actively reabsorbs SODIUM along with chloride. Its the diluting segment. In addition, LOW SODIUM DELIVERY TO DISTAL TUBULE CAN CAUSE RENIN RELEASE. so….my question is…if Atrial natriuretic peptide (ANP) causes an increase in gfr/brisk diureses/increase flow to nephron(as mentioned by colleagues on forums), and as a result, you decrease the time you have to reabsorb sodium, shouldn't the macula dense sense this as a DECREASE IN SODIUM AND THEREFORE INCREASE RENIN RELEASE?? I mean why the heck would the macula densa do the opposite and decrease its activity and decrease renin release
     
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  3. Apoplexy__

    Apoplexy__ Blood-and-thunder appearance Bronze Donor 2+ Year Member

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    1. Depends on the type of hypertension. You have the renin mechanism correct though. A few examples:
    -Essential hypertension: Thought to be a primary idiopathic retention of salt, increasing total body fluid. Therefore, renin is at a compensatory low.
    -Renal artery stenosis: Low flow coming through a stenotic artery is sensed, therefore the hypertension is a primary increase in renin.

    If you have a high renin HTN, that means the primary abnormality is the renin, and everything else is responding to that. If you have a low renin HTN, that means renin is subject to whatever the pathology is (increased aldosterone, vasopressors, etc.).

    Another thing that might help you out: "Increased sympathetic tone" can both increase and decrease renin:
    -If "sympathetic tone" = a1 receptors: a1 receptors directly decrease renin, and also cause vasoconstriction, indirectly causing renin to slowly decrease to compensate.
    -If "sympathetic tone" = B1 receptors: B1 receptors directly increase renin (receptors on JG cells).

    2. ANP and renin actually do oppose each other. ANP is released when BP and/or fluid volume needs to go down, and renin is released in the opposite conditions. Think about it -- ANP is released due to atrial stretching, so it only makes sense for it to cause things that would decrease atrial stretching.
     
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  4. abelabbot

    abelabbot Banned Banned Account on Hold 2+ Year Member

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    Yeah makes sense. Had to go over my basics to understand my first question.

    As far as my 2nd question, i knew i had the concept down actually...reading a post by someone else confused me a little...the physio they posted doesn't make sense...it's a lot simpler than that and yes your right..
     
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  5. CherryRedDracul

    CherryRedDracul 2 Chainz Muscular Dystrophy 2+ Year Member

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    FYI, ANP directly inhibits JG cells, so it directly hits the source of renin.
     

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