Renin/ACEI/ARB Question
Started by me454555
I believe it should go up. The renin that is there (and whatever will be released) is not being converted - some will be used to convert angiotensinogen, but as angio-I builds up, this conversion should decrease and renin should increase. At least that is my thought on it. What do others think?
I believe it would go up slightly but not signifigantly for 2 reasons.
1. SInce kidney is very well autoregulated i believe kidney blood flow would normalize shortly after starting an ACEI therefore blood flow would be normal through kidney and should keep renin at normal levels
2. however due to the loss of feedback by AN2 there woudl be an increase in renin due to loss of feedback. I think this is the only reason it is slightly elevated as i think the flow normalizes and therefore isnt a factor.
i dont know good question anyone else
1. SInce kidney is very well autoregulated i believe kidney blood flow would normalize shortly after starting an ACEI therefore blood flow would be normal through kidney and should keep renin at normal levels
2. however due to the loss of feedback by AN2 there woudl be an increase in renin due to loss of feedback. I think this is the only reason it is slightly elevated as i think the flow normalizes and therefore isnt a factor.
i dont know good question anyone else
Ramoray said:
Ok just thinking here ------ I assume that you are using an ACE inhibitor because their renin was increased to begin with (I am not sure how useful they are if renin isn't the cause of the HTN). You say "Blood flow would be normal through kidney and should keep renin at normal levels" - I think that before this the blood flow through the kidney was high (not low) and there was still renin release. The point I think is that the whole mechanism for sensing what's normal is screwed-up. So ACEI would actually lower the blood flow through the kidney from baseline (granted it would be more "normal" now), but I would think the kidney would want to secrete out even more renin due to its thinking that there is an even lower flow. Thus I don't think that renin levels would normalize. If renin just normalized, then why not just discontinue the ACEI because then without renin there is no problem. I am still thinking that renin level would be high. But I don't know for sure either. Please continue.
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I jsut read in FA that renin increases due to loss of feedback by AN2 but curiuosly i also read how AN2I resets the baroreceptor response making the body not fire out sympathetic respon to the new low pressure which means less symp= less B1 stimulation of renin which would lower renin so i think it increases a bit but due to a bunch of other effects its probably not all that high.
Also just read it works in low and high renin populations so it is not only effective if one has high renin
Also just read it works in low and high renin populations so it is not only effective if one has high renin
Ramoray said:
Renin goes up. renin is the beginning product. It will be continued to be produced and thus builds up. and actually it goes up quite significantly. Enough so that one can't do a true kidney workup for secondary reasons for HTN without first withdrawing ACEI and ARB's.
texdrake said:
Yep. And remember, blacks typically have low-renin states, which is why Aces typically do not work as well in blacks
Most efficacious
Whites = A + B (ace and beta)
Blacks = C + D (ca-blockers and diuretics)
Idiopathic said:
a nejm paper last fall showed that hydralazine and disorbium nitrate (sp?) works especially well in blacks. This paper was one of the first in a field called 'race-based therapeutics'. Some believe that african-americans' hypertension is related to salt sensitivity, derived from the selective pressures of limited salt conditions in Africa.
This is true, blacks are notorious for having low-renin HTN, and evidence will likely show that they have an actual genetic difference in salt transport when compared to whites (asians, et al)
