- Joined
- Mar 7, 2012
- Messages
- 94
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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
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