Urate and p-aminohippurate transport in isolated kidney tubules of normal and hyperuricemic chickens.
Urate and p-aminohippurate accumulations of kidney tubule fragments were studied in 5- to 6-week-old normal (LUA) and hyperuricemic (HUA) chickens. Tubules from LUA chicks consistently accumulated two to three-fold as much urate and p-aminohippurate as tubules from HUA chicks and thus confirmed the tubular origin of the urate transport defect in HUA chickens. A sodium gradient was required for optimal urate and p-aminohippurate accumulations and ouabain inhibited the accumulations of both compounds. Similar responses of urate and p-aminohippurate to treatments and reciprocal inhibitions between these compounds suggest that urate and p-aminohippurate are accumulated through a shared transport system.
D000618:Aminohippuric Acids / Q000378:metabolism*; D000818:Animals; D002645:Chickens; D066298:In Vitro Techniques; D007684:Kidney Tubules / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008320:Maltose / Q000378:metabolism; D008661:Metabolism, Inborn Errors / Q000378:metabolism*; D010101:Oxygen Consumption; D012016:Reference Values; D014527:Uric Acid / Q000378:metabolism*; D010130:p-Aminohippuric Acid / Q000378:metabolism*
D000618:Aminohippuric Acids; D014527:Uric Acid; D008320:Maltose; D007770:L-Lactate Dehydrogenase; D010130:p-Aminohippuric Acid