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Old 05-19-2014
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Default NBME 13 renin angiotensin aldosterone concept help

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 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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Old 05-19-2014
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NVMD..figured it out...sigh some of the people twisting concepts around and confusing others lol...thank god for wikipedia
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Old 05-20-2014
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Hello there.
Your post reminded me of something I read in the goljan notes (and other places) about the HTN mechanism and that not all types of HTN curse with high renin, actually the basic mechanism curses with low renin. There are other anomalies that causes HTN and high renin.

But since you already figured it out it would be nice if you could share your conclusions/thoughts.
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