A reduction in glomerular filtration rate (GFR) is a primary characteristic
of ischemic acute renal failure. The present study was undertaken to exami
ne the roles of angiotensin II, tubuloglomerular-feedback (TGF) mechanism,
and tubular obstruction for the GFR reduction in the postischemic kidney. R
enal ischemia was induced by occlusion of the bilateral renal arteries for
60 min, and renal function was examined at 2 and 24h after the onset of ref
low. After the end of 2-h reflow, the GFR was not significantly changed, bu
t the urine flow increased significantly. On the other hand, at the end of
24-h reflow, the GFR and urine flow decreased markedly along with increased
filtration fraction. The renal blood flow significantly decreased at 24 h,
but not 2 h, after reflow, which was accompanied by increased total renal
vascular resistance. Furosemide infusion (1 mg/min/kg) after 24h of reflow
prevented the reduction in GFR and filtration fraction without no changes i
n renal blood flow and total renal vascular resistance. Pretreatment of ena
lapril and losartan did not prevent the reduction in GFR, indicating that a
ngiotensin II was not involved. In morphological examinations, tubular obst
ruction was seen in the proximal and distal tubules of kidneys both at 2 an
d 24h after the onset of reflow. In two rabbits subjected to 48h of reflow,
the tubular obstruction was not observed, despite GFR remained depressed.
These results suggest that the late reduction in GFR in postischemic kidney
s is not mediated by angiotensin II, but is mediated, at least in part, by
the TGF mechanism. The tubular obstruction may be not prerequisite for the
GFR reduction in rabbits.