Effects of D-glucose on oxygen consumption of renal cortex suffering from ischemic injury

Alterations of Na(+)-dependent D-glucose transport in the proximal tubules resulting from ischemic injury were investigated. We measured the cortical oxygen (O2) consumption at various concentrations of exogenous D-glucose 1 day after ischemic injury in a kidney in which ischemia was induced by complete unilateral renal artery occlusion for 60 minutes and in a contralateral non-ischemic (control) kidney. Both kidneys exhibited a D-glucose concentration-dependent increase in O2 consumption. The increases in O2 consumption in both kidneys exhibited Michaelis-Menten-type saturation kinetics. However, increased Km and decreased Vmax were observed in the ischemic kidney. Phlorizin significantly inhibited O2 consumption in both kidneys at 5 mM, but the effect was not significantly at 0 mM of D-glucose. In contrast, ouabain significantly inhibited O2 consumption in both kidneys at 0 and 5 mM of D-glucose. The level of O2 consumption inhibition by phlorizin and ouabain in the ischemic kidney was markedly less than in the control kidney. The present study demonstrated that the decreased Na(+)-dependent D-glucose transport capacity can be attributed to a reduction in both phlorizin-sensitive transport capacity for D-glucose and ouabain-sensitive Na+, K(+)-ATPase activity 1 day after 60 minutes of ischemia.