AJP - Renal Physiology, Vol 248, Issue 6 804-F809, Copyright © 1985 by American Physiological Society
Renal sodium reabsorption, oxygen consumption, and gamma-glutamyltransferase excretion in the postischemic rat kidney
D. Herminghuysen, C. J. Welbourne and T. C. Welbourne
The effect of 30 min of renal artery occlusion on renal sodium
reabsorption, oxygen consumption, and brush border integrity was studied in
the immediate 1-h reflow period. Rats were studied using clearance and
renal extraction measurements. Glomerular filtration rate and renal plasma
flow were measured over four consecutive 15-min periods; renal venous
samples were drawn via an indwelling catheter. Renal oxygen consumption
(QO2) was calculated from renal blood flow, corrected for urine flow, and
from blood oxygen content measured with a fuel cell analyzer. Brush border
integrity was assessed by the excretion of the brush border marker enzyme
gamma-glutamyltransferase as well as by morphologic observation. Ischemia
induced a 10-fold rise in fractional sodium excretion in the initial 0- to
15-min period, rose to 20-fold during the subsequent two periods, 15-45
min, and then returned to the initial reflow period level. The progressive
deterioration of renal function with reflow could not be attributed to an
increase in the filtered Na+ load. Rather, Na+ reabsorption appeared to be
related to the presence of intact brush borders at 0-15 min, their removal
from the luminal surface between 15 and 45 min, and their return at 60 min
of reflow. Renal QO2 was coupled to Na+ reabsorption in the initial 15-min
and final 45- to 60-min reflow periods. However QO2 was significantly
increased over the control level at 30-45 min of reflow. The results point
to a significant role of brush border uptake in the development of
functional impairment following renal ischemia and suggest that the
associated rise in renal O2 consumption may be coupled to the reparation of
this organelle.
