In case of renal artery sclerosis we have only one regulatory mechanism - ATII constrict the efferent arteriole (see FA, p.458). In the other words "we" can't dilate afferent arteriole (because it sclerotic). So we can increase GFR/perfussion ONLY by constricting efferent arteriole by Angiotensin II.
If we will use ACE inhibitors we just block to conversion of AT to ATII and we will have lost control to renal perfusion.
Actually in some causes (may be in most) renal artery sclerosis is not well recognised.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1113401/
If we will use ACE inhibitors we just block to conversion of AT to ATII and we will have lost control to renal perfusion.
Actually in some causes (may be in most) renal artery sclerosis is not well recognised.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1113401/
