Abstract
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 V max value of tetraethylammonium uptake by brush-border membrane vesicles from reperfused kidneys was decreased compared with control, without any change in the K m value. The tetraethylammonium uptake by the vesicles from reperfused kidneys was decreased 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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