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Transport of tetraethylammonium, an organic cation has been studied using renal brush-border membrane vesicles isolated from rats with ischemic and ischemia-reperfusion injury. H+ gradient-dependent uptake of tetraethylammonium slightly, but significantly, decreased in brush-border membrane vesicles from ischemic kidneys. When the kidney was reperfused after ischemia, the extent of the decrease of tetraethylammonium uptake was much greater than that after ischemia alone. The Vmax value of tetraethylammonium uptake by brush-border membrane vesicles from reperfused kidneys was decreased compared with control, without any change in the Km value. The tetraethylammonium uptake by the vesicles from reperfused kidneys was decreases both in the presence and absence of the outward H+ gradient (driving force). Uptake of D-glucose in renal brush-border membrane vesicles was also decreased by ischemia and again, reperfusion caused a further decrease of the uptake. Reperfusion also induced marked changes in the enrichment and recovery of marker enzymes in the isolated brush-border membrane fraction compared with ischemia. These findings suggest that renal ischemic injury altered the transport properties of tetraethylammonium as well as D-glucose, and that reperfusion after ischemia induced further damages on these functions in the brush-border membrane.
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