Effect of trimethylamine and its homologues on renal conservation of trimethylamine oxide by the spiny dogfish, Squalus acanthias

Abstract

In renal clearance experiments with dogfish, trimethylamine HCL (TMA) administration (i.m.) results in a large increase in trimethylamine oxide (Oxide) excretion. This is shown to occur by inhibition of net renal tubular reabsorption of the Oxide. The TMA, on the other hand, reaches the urine by net tubular secretion in quantities which are consistent with the attainment of diffusion equilibrium across the pH gradient between urine and plasma. The effect of TMA is not related to increased urine flow but is a specific effect on Oxide reabsorption. The administration of the homologue of TMA, dimethylamine, results in a similar but less profound blockade of Oxide reabsorption. Methylamine, however, has no effect at all on Oxide reabsorption. Large excretory losses of TMAO occurred without any change in TMAO plasma level, further indicating the physiological regulation of the plasma concentration of this weak base.