Nephrology Dialysis Transplantation, Vol 12, Issue 5 899-903, Copyright © 1997 by Oxford University Press
H Haller, J Park, D Dragun, A Lippoldt and F Luft
How an increase in blood pressure, in and of itself, induces hypertensive
nephrosclerosis is unclear. In an earlier study we found that leukocyte
infiltration, proximal tubular cell proliferation, matrix deposition and
interstitial fibrosis occur in the unclipped kidney of 2 K 1 C Goldblatt
hypertensive rats. In this study we tested the hypothesis that the cell
surface adhesion molecule ICAM-1 is expressed on the vascular endothelium
and tubular epithelium of unclipped kidneys at 4 weeks. As a positive
control, we examined the clipped kidney as well. We found that systolic
blood pressure was significantly elevated in renovascular hypertensive rats
compared to sham-operated controls after 4 weeks (198 ± 5 mmHg
vs 121 ± 2 mmHg, P
<0.001). Furthermore, quantitative (densitometry) measurements
showed that ICAM-1 expression on vascular endothelium and on tubular cells
was significantly increased in unclipped kidneys compared to controls
(P <0.05). The same was true for monocyte and
granulocyte infiltration (P <0.05). These same
variables were even more prominent in the clipped kidneys, compared to
unclipped and control kidneys (P < 0.05). Our
data show that ICAM-1 is expressed in unclipped kidneys exposed to
hypertension as well as in clipped kidneys exposed to ischemia. We suggest
that mechanical injury induced by increased blood pressure is responsible
for an inflammatory adhesion molecule-mediated response and concomitant
renal injury. Keywords: renovascular hypertension;
hypertension-induced nephrosclerosis; adhesion molecules; ICAM
ORIGINAL ARTICLES
Leukocyte infiltration and ICAM-1 expression in two-kidney one-clip hypertension
Franz Volhard Clinic, Wiltberg Strasse 50, 13122 Berlin, Germany
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