AJP - Renal Physiology, Vol 250, Issue 2 357-F363, Copyright © 1986 by American Physiological Society
Adenine nucleotide metabolism and mitochondrial Ca2+ transport following renal ischemia
P. E. Arnold, V. J. Van Putten, D. Lumlertgul, T. J. Burke and R. W. Schrier
Mitochondrial Ca2+ accumulation and mitochondrial respiratory dysfunction
have been observed after renal ischemia. The present study examined the
effects of ischemia and reperfusion on cellular energy production and
mitochondrial Ca2+ transport after 50 min of bilateral renal artery and
vein clamping in the anesthetized rat. Prior to reflow, tissue ATP and
total adenine nucleotide levels were severely reduced. These nucleotide
levels recovered towards normal but remained lower than control values
throughout 24 h of reperfusion. Energy-linked mitochondrial Ca2+ uptake was
unmeasurable, mitochondrial Ca2+ efflux was increased and the mitochondria
were unable to maintain a steady-state free Ca2+ concentration prior to
reflow. Three hours of reperfusion was associated with a normalization of
mitochondrial Ca2+ uptake, release, and steady-state buffering. However,
progressive deterioration subsequently occurred in these processes. Thus
the mitochondrial Ca2+ accumulation previously observed during the later
stages of postischemic reperfusion (3-24 h) is due neither to an increase
in the rate of active Ca2+ uptake nor to a decrease in the rate of Ca2+
release. The present results therefore suggest that passive mitochondrial
Ca2+ accumulation may occur during the later stages of reperfusion,
probably due to a progressive increase in the cytosolic Ca2+ concentration.
