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pubmed-article:2316668pubmed:abstractTextRabbit renal brush-border membrane vesicles (BBMV) were used to study the transport of the cationic neurotoxin, 1-methyl-4-phenylpyridinium (MPP+). An outwardly directed H(+)-gradient stimulated MPP+ uptake and led to the development of an active accumulation of MPP+ within the vesicles. H(+)-gradient driven MPP+ transport was saturable, with a maximal transport rate of 3 nmol.mg-1.min-1 and an apparent Michaelis constant (Kt) of 8 microM. MPP+ and tetraethylammonium (TEA) behaved as competitive inhibitors of one another's transport in renal BBMV, suggesting the presence of a common transport pathway for these organic cations. At an ambient pH of 7.5, preloading BBMV with MPP+ failed to stimulate TEA uptake, although trans TEA did stimulate MPP+ uptake. Increasing ambient pH to 8.5 (i.e., reducing competition between H+ and these organic cations for a common transport pathway) led to a clear reciprocal trans stimulation of TEA and MPP+ fluxes. With an equilibrium-shift protocol, a trans concentration of MPP+ energized uphill transport of TEA. We conclude that MPP+ and TEA share a common organic cation-H+ exchange pathway in the renal brush border, although turnover of an MPP(+)-loaded exchanger is slow compared with that for a TEA or H(+)-loaded exchanger.lld:pubmed
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pubmed-article:2316668pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:2316668pubmed:articleTitleMPP+ is transported by the TEA(+)-H+ exchanger of renal brush-border membrane vesicles.lld:pubmed
pubmed-article:2316668pubmed:affiliationDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson 85724.lld:pubmed
pubmed-article:2316668pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2316668pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed