THE ACTION OF SODIUM FLUOROACETATE ON THE RENAL TUBULAR TRANSPORT OF PARA-AMINOHIPPURATE AND GLUCOSE IN THE DOG

¹ Department of Pharmacology, State University of New York, Upstate Medical Center, Syracuse 10, New York

In anesthetized dogs sodium fluoroacetate (NaFAc) reduced renal blood flow, para-aminohippurate, (R.P.F.), creatinine and inulin clearance (GFR) as well as para-aminohippurate and glucose transport maximum (PAH Tm, glucose Tm). Infusions of sodium acetate increased PAH Tm and protected against the effects of sodium fluoroacetate on the PAH secretory mechanism. Once fluoroacetate effects had occurred acetate had no stimulatory effect on PAH Tm. The evidence presented suggests a competitive mechanism between NaFAc and sodium acetate on the PAH secretory mechanism. Kidney slices from fluoroacetate poisoned dogs show a reduction in their ability to concentrate PAH both in the absence and presence of sodium acetate as substrate.

Glucose Tm is reduced by fluoroacetate administration. It differs from the PAH secretory mechanism in that sodium acetate does not protect the glucose reabsorptive mechanism against sodium fluoroacetate effects. The renal hemodynamic changes produced by NaFAc make it difficult to interpret these effects on glucose Tm. It is possible that a part of the fluoroacetate induced reduction in glucose Tm is due to a blocking of renal tubular reabsorption of glucose.