Abstract

The renal tubular transport and metabolism of nicotinic acid (NA) were investigated using the Sperber technique in unanesthetized hens. Infusion of [14C]NA into the avian renal portal circulation at 10(-10) mol/kg/min revealed that the 14C label was actively transported into urine at a rate 74% that of simultaneously infused tetraethylammonium. Increases in NA infusion rates enhanced 14C label transport so that it eventually equalled the excretion rate of tetraethylammonium. At a NA infusion rate of 10(-8) mol/kg/min, this transport was not affected by probenecid, pyrazinoic acid or p-aminohippurate. Above infusion rates of 10(-7) mol/kg/min, saturation of 14C label transport was reached. Electrophoretic analysis of the 14C label excreted in urine at NA infusion rates less than 10(-7) mol/kg/min revealed a single, unidentified metabolite. At infusion rates greater than 10(-7) mol/kg/min, both the radiolabeled metabolite and [14C]NA were found in the urine. We conclude that NA is transported by a specific mechanism into the avian tubule cell where it is metabolized. As the body's load of this vitamin increases, NA is excreted first in the form of a metabolite and then as both metabolite and unutilized NA.