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AJP - Renal Physiology, Vol 249, Issue 5 654-F661, Copyright © 1985 by American Physiological Society
ARTICLES |
A. M. Kahn, H. Shelat and E. J. Weinman
We examined the transport of urate in basolateral membrane vesicles from the rat kidney and determined the relationship between the transport of urate and p-aminohippurate (PAH). Urate was not converted to allantoin, and the uptake of urate represented transport into an osmotically active intravesicular space. The 10-s uptake of 53 microM [14C]urate in basolateral vesicles was inhibited 39 +/- 6, 49 +/- 10, and 35 +/- 3% by (in mM) external 2.4 probenecid, 2.4 DIDS, and 1.4 unlabeled urate, respectively. The 10-s uptake of 353 microM [14C]urate was trans-stimulated 82 +/- 8% by preloading basolateral vesicles with 1.5 mM unlabeled urate. The uptake of urate was stimulated by an outwardly directed gradient for Cl- (Cl-in = 25 mM, Cl-out = 5 mM). This effect was not consequent to a more electropositive intravesicular space, as monitored by the voltage-sensitive sodium-L-malate cotransport system. The Cl- gradient-stimulated component of urate uptake in basolateral vesicles was not cis-inhibited by 4.8 mM PAH, whereas Cl gradient-stimulated urate uptake in brush border vesicles was cis-inhibited 43 +/- 5% by PAH. In the absence of Cl-, 4.8 mM PAH did not cis-inhibit, and 5.4 mM PAH or 6.4 mM lactate did not trans-stimulate the uptake of urate in basolateral vesicles, contrasting with results obtained with brush border vesicles. The uptake of urate in basolateral vesicles was not stimulated by external Na+ relative to K+, Li+, or Cs+. In contrast, PAH uptake in basolateral vesicles was stimulated 87 +/- 9% by external Na+.(ABSTRACT TRUNCATED AT 250 WORDS)
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