• 1 January 1976
    • journal article
    • research article
    • Vol. 199  (3) , 498-509
Abstract
Preparation and incubation of renal cortical slices from adult, female, New Zealand white rabbit depleted tissue citrate concentration. Acetate (10.0 mM) in the incubation significantly increased slice citrate concentration and p-aminohippurate (PAH) accumulation. Physiological concentrations of citrate increased PAH accumulation and final medium pH. Increasing concentrations of citrate produced a biphasic effect on PAH accumulation. Citrate acted as an intracellular modulator of organic anion transport. This hypothesis was tested with other stimulators of PAH accumulation. Physiological concentrations of .alpha.-ketoglutarate or succinate increased slice accumulation of PAH. Higher concentrations of either substrate significantly inhibited PAH accumulation. Final medium pH increased with increased medium concentration of both substrates. .alpha.-Ketoglutarate (0.5 mM) increased PAH accumulation but had no effect on slice citrate concentration. Glucose did not alter either PAH accumulation or slice citrate concentration. Slices incubated without substrate were depleted of citrate but not of .alpha.-ketoglutarate. Acetate (1.0 mM) significantly increased slice concentration of both .alpha.-ketoglutarate and citrate. Organic anion transport was modulated by several metabolic intermediates acting through similar but separate mechanisms.