Excretion of ammonia injected into renal artery

Abstract

Certain characteristics of the ammonia secretory mechanism in the dog have been studied by the method of Chinard. Ammonium chloride or acetate and creatinine were rapidly injected into one renal artery and a series of urine samples were collected separately from the two ureters. In acidosis, injected ammonia appears in the urine earlier than does creatinine, indicating that some fraction enters the tubule from the blood downstream from the glomerulus. The maximum rate of excretion of ammonia relative to the dose administered is usually less than that of creatinine, indicating that filtered ammonia is in part reabsorbed from the tubular urine. Finally, the excretion of ammonia is much prolonged relative to creatinine, indicating that it continues to be added to the tubular urine from cellular stores built up from both filtrate and peritubular blood. In alkalosis, the time course of excretion of creatinine is unchanged from that observed in acidosis. However, the excretion of ammonia is abolished. That which enters the tubule in the filtrate is completely reabsorbed. These data are consistent with the view that ammonia diffuses freely in both directions across the renal tubular epithelium as free base and distributes among tubular urine, tubular cells, and peritubular blood in accordance with their respective hydrogen ion concentrations.