Elucidating the precise mechanism of intestinal ammonium transport is critical to the understanding of the acidosis associated with intestinal urinary diversion. Unfortunately, it is incompletely understood and controversial. Recently, we have shown that furosemide and Ba2+ significantly inhibit ammonium absorption in the ileum. On the basis of this and other data, we have suggested that ionized ammonium absorption occurs via K(+)-transport pathways. The present study examines intestinal ammonium absorption and its inhibition by K+ and Ba2+ utilizing a simplified in vivo system in rat distal ileum. Ammonium absorption demonstrates a tendency towards saturation at initial concentrations between 0 and 300 mM/l. Above 300 mM/l. there was a marked increase in ammonium absorption suggesting a possible biological effect of high NH4+ concentrations on the intestinal segment. Potassium inhibits ammonium absorption. K+ (50 mM/l.) significantly inhibited ammonium at an initial concentration of 100 mM/l. (p less than 0.05) and K+ (100 mM/l.) inhibited ammonium absorption at both 50 and 100 mM/l. (p less than 0.05 and p less than 0.01 respectively). Potassium inhibition of ammonium absorption was lost at concentrations above 200 mM/l. suggesting that K+ inhibition occurs via a competitive mechanism. Ba2+ (25 mM/l.) was shown to be a potent inhibitor of ammonium absorption. This significant inhibition persisted at high initial ammonium concentrations suggesting a complex, noncompetitive mechanism of inhibition. In conclusion, this study provides important data further suggesting that ammonium transport in the intestine occurs via K+ transport pathways, and suggests that the traditionally held mechanism of nonionic ammonium diffusion needs reevaluation.