Nonesterified fatty acid uptake by dog kidney: effects of probenecid and chlorothiazide

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Abstract
Net renal nonesterified fatty acid uptake (QNEFA) was studied to determine whether the organic acid (e.g., PAH [p-aminohippurate]) transport mechanism participates in transport or metabolism of NEFA in renal tubular cells. In 12 experiments QnefA was measured in anesthetized (pentobarbital) dogs during the infusion of a substrate of the PAH transport mechanism, probenecid, or chlorothiazide. Under control conditions QNEFA was proportional to NEFA arterial levels [NEFA]A. Mean control Qnefa was 132[plus or minus].03 (SE) [mu]eq/min. g kidney at a mean [NEFA]A. of 570 [plus or minus] 63 [mu]eq/1. During probenecid infusion QNEFA decreased to -.042 [plus or minus] .032 [mu]eq/min. g in spite of a rise in mean [NEFA]A to 848 [plus or minus] 102 [mu]eq/l. Chlorothiazide decreased QNEFA to [plus or minus] .005[plus or minus]J015 [mu]eq/min. g. The significant correlation observed between Na reabsorption and QNEFA under control conditions was lost during chlorothiazide infusion. These observations are consistent with the participation of the renal organic acid transport system in the entry and/or utilization of endogenous renal substrates such as NEFA. The possible utilization of the energy derived from NEFA in supporting active transport of Na is discussed.