[The renin-angiotensin system in diabetic patients]

We review available data on the activity of the renin-angiotensin system (RAS), responsiveness to angiotensin II (ANG II), ANG II receptor number, and effects of inhibition of the RAS by angiotensin I converting enzyme (ACE) inhibitors in patients with diabetes mellitus. Most authors, including ourselves, observed a normal or enhanced activity of the RAS in metabolically stable diabetics. Increased but also reduced activity of the RAS was described in nephropathic diabetes. This is in contrast to the common suggestion that the RAS of diabetics is generally suppressed and functionally inactive. The last assumption was mainly based on the finding of reduced ANG II receptor numbers in anorectic, severely hyperglycemic rats. These findings could not be reproduced in man, and a higher ANG II receptor concentration on platelets of diabetics goes in parallel with the frequent finding of an enhanced pressor response to infused ANG II in diabetes. This increased responsiveness is most probably of functional importance since the RAS is not suppressed - as one would expect - in the face of a supranormal body sodium content. A number of data also indicate that renal resistance vessels display increased responsiveness to ANG II in diabetics. This may be a reason for hyperfiltration. This notion is further supported by the reduction of albuminuria which is usually observed following inhibition of the RAS with ACE inhibitors, and which may be an index of reduction of glomerular capillary pressure in human diabetes.