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Senior Member
Join Date: Mar 2008
Posts: 374
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This is uworld question 691 if anyone is curious.
Basically, a man is being treated with an ARB. "His blood pressure decreases to NORMAL VALUE over SEVERAL WEEKS OF TREATMENT. Hes compliant and no side effects. Its your classic what goes up what goes down...but... the correct answer is -no change in bradykinin (obvious, ARB doesn't affect ACE) -decrease in aldosterone (obvious because angiotensin II can't stimulate aldosterone) BUT I got stumped because I thought with weeks of treatment and normal blood pressure, that renin, angiontensin I and angiotensin II would all be decreased.. But apparently the answer is renin increased, angiotensin I increased, and angiotensin II increased. How is that possible? My understanding of the regulation of the RAAS system is that angiontensin II itself feeds back, and a long feedback loop based on sodium concentration, blood pressure, blood volume. The explanation says ARBS intefere with teh negative feedback mechanism...which mechanism? Angiotensin II is produced normally because ACE is fine, it should feedback. PLUS the dudes pressure is normal, and hes been on this stuff for weeks, why the heck is renin still increased, angiontensin 1 increased, and angiotensin II increased?????? Is tehre some huge flaw in my reasoning? Edit: I guess I didn't understand that ARBS competitively block angiontesin 1 receptors, thereby stopping the feedback at the level of the JG cells..but still even after a few weeks of controlled BP renin is still high huh...weird.....so the block on AT-1 overpowers normalized BP? Last edited by herewego; 05-10-2012 at 08:33 PM. |
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