Twenty paired samples of arterial and renal venous plasma, collected simultaneously from dogs in ammonium chloride acidosis, were analyzed by column chromatography for 23 α-amino acids. Fifteen additional paired samples from dogs in acute metabolic alkalosis were similarly analyzed. In ammonium chloride acidosis, glutamine plus asparagine, glycine, citrulline, tryptophan, and proline are extracted from renal blood plasma. Alanine, serine, glutamic acid, cystine, and ornithine are added to renal venous plasma. The addition of glutamic and aspartic acids amounts only to 4% of the extraction of glutamine plus asparagine. It is, therefore, probable that both α-amino and amide nitrogens are removed from the parent amide molecules. In acute metabolic alkalosis, the extraction of glutamine plus asparagine is halved, on an average. The extraction of glycine and the addition of alanine and serine are essentially unchanged. Therefore, only the extraction of glutamine plus asparagine varies to a quantitatively significant degree with changes in acid-base balance which markedly alter the rate of excretion of ammonia.

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The nature and mechanism of the diuresis produced in the dog by strophanthidin was investigated by infusion of the drug into one renal artery. Saline-loaded dogs respond to strophanthidin infusion with a prompt fall in glomerular filtration rate (GFR) and a delayed saluresis and diuresis. The effect on electrolyte transport can be blocked by loading with potassium salts but the fall in GFR can be only partially prevented. Strophanthidin given to adrenalectomized dogs produces the same effect as in the intact animal. The ability to maintain a steep transtubular hydrogen ion concentration gradient is severely impaired. The data are best interpreted as inhibition of the potassium arm of a linked Na-K exchange across the peritubular cell membrane, with diuresis occurring secondary to this block. Impairment of the ability to maintain a steep hydrogen ion concentration gradient indicates an additional effect on linked exchange occurring at the luminal surface of the cell.

Ammonium lactate and a variety of amides and amino acids were infused into one renal artery of anesthetized dogs in acidosis. Urine was collected separately from the two kidneys and rates of excretion of ammonia on the two sides were compared. The infusion of ammonium lactate resulted in a prompt increase in ammonia excretion restricted to the side infused. As much as 50% of the infused ammonia appeared as excess ammonia in the urine. The infusion of glutamine, asparagine, alanine, glycine, leucine, and glutamic acid induced bilateral increases in rates of ammonia excretion, commonly greater on the side infused. However, ammonia excretion increased significantly on the side contralateral to that infused. A much smaller fraction of the infused nitrogen appeared as urinary ammonia than when ammonium lactate was infused. The infusion of valine induced no increase in ammonia excretion by either kidney; rather, ammonia excretion was reduced. The significance of these results in relation to the study of renal metabolism of N15 compounds is discussed.

Sodium movements in internally perfused giant axons from the squid Dosidicus gigas were studied with varying internal sodium concentrations and with fluoride as the internal anion. It was found that as the internal