Participation of Monocarboxylic Anion and Bicarbonate Exchange System for the Transport of Acetic Acid and Monocarboxylic Acid Drugs in the Small Intestinal Brush-Border Membrane Vesicles

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A participation of bicarbonate exchange system for the transport of acetic acid and the related monocarboxylic acid drugs in the intestinal brush-border membrane vesicles (BBMVs) was investigated. The uptake of [^3H] acetic acid at 37℃ by BBMVs was markedly stimulated and showed a clear overshoot phenomenon in the presence of outward-directed bicarbonate gradient (pH_<in> = 7.5,[KHCO_3]_<in> or [NaHCO_3]_<in> = 100 mM ; pH_<out> = 7.5,[K-gluconate]_<out> or [Na-gluconate]_<out> = 100 mM). This uptake process was saturable (K_t = 50.4±4.96 mM and J_<max> = 11.6±0.61 nmol/mg protein/10 s) and was inhibited by DIDS (4,4-diisothiocyano-2,2'-disulfonic acid stilbene disodium salt) and furosemide, anion exchange inhibitors, and by many monocarboxylates. The initial uptake of [^3H] acetic acid was competitively inhibited by salicylic acid, suggesting the common transport between acetic acid and salicylic acid. At lower extravesicular pHs and in the presence of outward-directed bicarbonate gradient (pH_<in> = 7.5,[KHCO_3]_<in> = 100 mM ; pH_<out> = 6.0 or 5.0,[K-gluconate]_<out> = 100 mM) where membrane potential was clamped to zero by K^+-valinomycin, the uptake of [^3H] acetic acid showed an overshoot phenomenon, whereas the uptake was significantly decreased in the presence of carbonyl cyanide p-trifluoromethoxyphenylhydrazone, a protonophore. It was concluded, therefore, that there are one or two mechanisms for the carrier-mediated transport of acetic acid and monocarboxylates related to bicarbonate exchange systems in rabbit intestinal BBMVs : 1) proton gradient independent and bicarbonate exchange system ; 2) proton gradient dependent and bicarbonate exchange system.

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