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.
Department of Physiology II, Niigata University School of Medicine, Japan.
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Kuramochi
D000818:Animals; D001692:Biological Transport; D005947:Glucose / Q000493:pharmacokinetics / Q000494:pharmacology*; D007511:Ischemia / Q000378:metabolism*; D007672:Kidney Cortex / Q000098:blood supply* / Q000378:metabolism*; D008297:Male; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
D005947:Glucose