Intoxication with 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) results in marked increases in cellular smooth endoplasmic reticulum content and microsomal drug metabolizing enzyme activity in kidney cortex. Therefore, it was of interest to determine the effect of TCDD on several proximal tubular functions. Adult rats were treated with 10, 25, and 50 μg/kg, intraperitoneally, or 1 and 5 μg, intragastrically, TCDD. Neither intragastric dose of TCDD had a significant effect on the ability of renal cortical slices to accumulatep‐aminohippuric acid (PAH) 7 days after treatment. Similarly, 10 μg/kg TCDD 3 or 7 days after treatment did not affect PAH accumulation.N‐methylnicotinamide (NMN) accumulation was slightly decreased following this treatment. At 25 μg/kg, TCDD decreased the capacity of renal tissues to transport both PAH and NMN 7 days after exposure. Accumulation of 2‐deoxyglucose was unaffected by TCDD. The increase in ammoniagenesis and gluconeo‐genesis observed in acidotic states was not significantly different in animals that had been treated with 25 μg/kg TCDD 7 days before experimentation. Glomerular filtration rate and effective renal plasma flow were decreased in rats after 25 or 50 μg/kg TCDD. Volume expansion did not alter this relationship. Fractional sodium excretion was less than 1% in both control and TCDD‐treated animals. With volume expansion sodium excretion increased to approximately 5% and was not different for control and TCDD‐treated animals. The effect of TCDD on renal function is, therefore, most likely a result of general toxicosis rather than specific functional lesions.