H. Haller et al., LEUKOCYTE INFILTRATION AND ICAM-1 EXPRESSION IN 2-KIDNEY ONE-CLIP HYPERTENSION, Nephrology, dialysis, transplantation, 12(5), 1997, pp. 899-903
How an increase in blood pressure, in and of itself, induces hypertens
ive nephrosclerosis is unclear. In an earlier study we found that leuk
ocyte infiltration, proximal tubular cell proliferation, matrix deposi
tion 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 vas
cular endothelium and tubular epithelium of unclipped kidneys at 4 wee
ks. As a positive control, we examined the clipped kidney as well. We
found that systolic blood pressure was significantly elevated in renov
ascular hypertensive rats compared to sham-operated controls after 4 w
eeks (198 +/- 5 mmHg vs 121 +/- 2 mmHg, P < 0.001). Furthermore, quant
itative (densitometry) measurements showed that ICAM-1 expression on v
ascular endothelium and on tubular cells was significantly increased i
n unclipped kidneys compared to controls (P < 0.05). The same was true
for monocyte and granulocyte infiltration (P < 0.05). These same vari
ables were even more prominent in the clipped kidneys, compared to unc
lipped and control kidneys (P < 0.05). Our data show that ICAM-1 is ex
pressed in unclipped kidneys exposed to hypertension as well as in cli
pped kidneys exposed to ischemia. We suggest that mechanical injury in
duced by increased blood pressure is responsible for an inflammatory a
dhesion molecule-mediated response and concomitant renal injury.