Effect of Renal Ischaemia on Organic Compound Transport in Rabbit Kidney Proximal Tubule

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Abstract
This study was carried out to determine the effect of renal ischaemia on transport systems for organic compounds in the rabbit kidney proximal tubule. Ischaemia for 30 or 60 min. induced glucosuria and phosphaturia, which was accompanied by polyuria and natriuresis. The Na+‐dependent uptake of glucose, succinate and L‐glutamate by brush‐border membrane vesicles was not altered by 30 or 60 min. of ischaemia, while the H+/tetraethylammonium antiport was significantly inhibited after 30 min. of ischaemia. When the duration of ischaemia was extended to 120 min. the uptake of glucose and succinate by brush‐border membrane vesicles was also significantly attenuated, but the L‐glutamate uptake was not altered. The uptake of glucose, succinate and L‐glutamate by basolateral membrane vesicles was not impaired even with 120 min. of ischaemia, suggesting that transport systems for organic compounds in the brush‐border membrane are more sensitive to ischaemia than those in the basolateral membrane. Ouabain‐sensitive oxygen consumption in renal cortical slices was not depressed by 60 min. of ischaemia. When kidneys were reperfused for 60 min. following 60 min. of ischaemia, the Na+‐glucose and Na+‐succinate cotransport and the H+/tetraethylammonium antiport were not different from the control, but the recovery of alkaline phosphatase was significantly reduced. When kidneys were subjected to ischaemia for 60 min., a loss of brush‐border microvilli and plasma membrane was observed after 5 or 60 min. of reflow in the proximal convoluted tubule. After 3 hr of reflow, focal necrosis appeared although the microvilli were partially regenerated. These results indicate that renal ischaemia induces selective impairments of transport systems in the rabbit renal proximal tubule, and that the glucosuria and phosphaturia induced by transient ischaemia are results, at least in part, from a diminution of brush‐border surface area rather than a direct defect in the function of the membrane transport systems.

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