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

  • KURAMOCHI GEN
    Department of Physiology II, Niigata University School of Medicine

抄録

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 ichemia 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 5mM, but the effect was not significant at 0mM 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 Natdependent 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 ischemic.

収録刊行物

詳細情報 詳細情報について

  • CRID
    1390282679834894336
  • NII論文ID
    130004170110
  • DOI
    10.14842/jpnjnephrol1959.36.1240
  • ISSN
    18840728
    03852385
  • PubMed
    7853755
  • 本文言語コード
    en
  • データソース種別
    • JaLC
    • PubMed
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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