Renal Synthesis, Degradation and Active Transport of Aliphatic Acyl Amino Acids

Abstract

Active accumulation of PAH by kidney slices of rabbit, dog, guinea pig and pigeon is enhanced by acetate and inhibited by fatty acids of intermediate carbon chain length (C6-C12). Synthesis of aromatic and aliphatic (C2-C12) acylglycines, via acyl thioesters of coenzyme A, was demonstrated in kidney slices and acetone powder extracts from these spp. The C2-C4 acylglycines have little effect on PAH accumulation, while the C5-C8 derivatives are actively accumulated and are potent competitive inhibitors. Acetate has no effect on PAH transport in chicken, duck, turkey, or goose, spp. in which the kidney cannot conjugate glycine. Presumably inhibition by fatty acids of intermediate chain length results from synthesis of competitive aliphatic acylglycines; PAH transport may be continuously suppressed by such compounds arising from endogenous sources. A basis for the stimulatory effect of acetate is presented in relation to the glycine conjugation reactions. Synthesis of acyl-L-alanines in rabbit kidney accounts for inhibition of PAH transport by L-alanine in that sp.