Nephrology Dialysis Transplantation, Vol 13, Issue 1 173-176, Copyright © 1998 by Oxford University Press
A Nabokov, K Amann, P Gassmann, U Schwarz, S Orth and E Ritz
Background: Angiotensin-converting enzyme (ACE)
inhibitors have been shown to ameliorate the progression of
glomerulosclerosis both in experimental models of uraemia and in patients
with renal failure. It has not been documented, however, whether this sis
due to a decrease in angiotensin II generation or is a consequence of
elevated local level of bradykinin. Methods:
Morphometric investigation of renal tissue was performed in 5/6
nephrectomized (SNx) rats, i.e. untreated or treated with the ACE inhibitor
ramipril (SNx-RAM), the B2 kinin receptor antagonist HOE 140 (SNx-HOE), or
a combination of both (SNx-RAM + HOE) over 8 weeks. A further group of SNx
received delayed treatment with ramipril from week 5 onward (SNx-RAMD). In
addition, a sham-operated (SHAM) control group was studied.
Results: Systolic blood pressure was significantly
lower in both SNx-RAM and SNx-RAM + HOE groups compared to (untreated) SNx.
The glomerulosclerosis index (GSI) was substantially higher in the
(untreated) SNx group (0.24±0.04) vs SHAM
(0.02±0.01). A significantly higher GSI was found in the SNx-HOE
group (0.45±0.08) as compared to (untreated) SNx. However, in
the SNx-RAM, SNx-RAM + HOE, and SNx-RAMD groups, the GSI was lowered to a
similar extent (0.1±0.02, 0.09±0.02, and
0.07±0.01 respectively). In addition, a concomitant attenuation
of tubulointerstitial damage was noted in all the above groups.
Conclusion: Increased kinin activity does not appear
to play a major role in the renoprotective effect of ACE inhibitors in the
remnant kidney model. Key words:
angiotensin-converting enzyme inhibitor; bradykinin; renal failure; remnant
kidney model; glomerulosclerosis
BRIEF REPORTS
The renoprotective effect of angiotensin-converting enzyme inhibitors in experimental chronic renal failure is not dependent on enhanced kinin activity
Department of Internal Medicine and Institute of Pathology, University of Heidelberg, Bergheimer Str. 56A, D-69115 Heidelberg, Germany
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