The mechanism whereby high CO2 tensions are formed in the urine has been the subject of considerable debate. Pitts and Alexander (1) proposed that the CO2 tension in alkaline urines is increased as a result of the following sequence: 1) increased delivery of NaHCO3 to the distal tubule; 2) increased formation of HCO3 as a result of a Na+-H+ exchange in this segment; 3) MATERIALS AND METHODSA total of 27 experiments were performed on normal young adults (medical students, house officers and student nurses) after an overnight fast.Maximum water diuresis was maintained by the rapid intravenous infusion of either 5 per cent dextrose or 5 per cent fructose in water. The subjects remained recumbent throughout the experiments except for those individuals from whom voided urine specimens were obtained. Urine collection periods of 15 to 20 minutes were employed; the samples were collected under mineral oil by direct voiding in some experiments, by indwelling catheter in most. At the mid-point of each urine collection period blood was drawn into heparinized, oiled syringes from an indwelling needle in either a brachial or femoral artery.Blood and urine pH were anaerobically determined immediately with a Cambridge pH meter with the electrode assembly housed in an incubator at a constant temperature of 370 C. Plasma and urine CO2 content were determined by the method of Van Slyke and Neill (4). Bicarbonate concentration and pCO2 were calculated from the Henderson-Hasselbalch equation. The pK, of H2C08 in urine was estimated for each sample according to the formula: pK, = 6.33 -0.5 -1B, where B represents the total cation concentration of the sample in question (5).It was assumed that the sum [Na+]+ [K+] was equal to at least 95 per cent of [B+]. It was found that the arbitrary selection of a pK1 of 6.10 introduced a variable error of considerable magnitude when calculating pCO2 in urines of varying pH and bicarbonate concentration.However, using the pK, estimated from 6.33 -0.5 -/B, close agreement was obtained between calculated pCO2 and tonometrically determined pCO2. The conventional proportionality constant of 0.0309 was used to convert[H2COJ] to pCO2. For plasma, a pK1 of 6.10 and a proportionality constant of 0.0301 were used.Inorganic phosphate in urine was determined by the method of Fiske and Subbarow (6). Titration curves for urines obtained during several of the experiments were determined as follows:Ten ml. urine was acidified to < pH 2.0 by the addition of 0.1 HCl. Following vigorous stirring for 15 minutes (to dispel generated CO2), the samples were titrated to pH 6.0 to 6.2 with 0.1 N NaOH. Further titration to pH > 8.0 was performed with 0.01 N NaOH which was 770

To examine the adequacy of the mixing hypothesis as an explanation for high urinary CO2 tensions, urine-plasma pCO2 gradients were examined in normal subjects receiving NaHCO3 infusions in whom urinary buffer concentration was minimized by solute and water diuresis, antecedent carbohydrate diet and glucose infusions. U-P gradients varying from 23 to 78 mm Hg were generated in the face of minimal urinary buffer concentrations which varied from 1.40 to 2.95 mEq/l. Only by the most extreme assumptions, i. e. maximal heterogeneity and no back-diffusion of CO2, could the mixing hypothesis account for the observed gradients. Since these assumptions were highly improbable, it was concluded that the mixing hypothesis is not a tenable explanation of the high CO2 tension of alkaline urine.

The reabsorption of filtered HCO3-by the kidney is thought to result not from the active reabsorption of HCO3-ions but rather from the secretion of cellular H+ in exchange for tubular Na+ (1,2

Urinary magnesium excretion was evaluated during the administration of magnesium salts into one leg vein of the chicken by means of the Sperber technique. Changes of magnesium excretion paralleled those of filtered load and sustained unilateral differences of magnesium excretion were not observed. Corrected magnesium-inulin clearance ratios rose to values of approximately 1.0 and remained at that level despite continuing rises of filtered load. The results indicate that magnesium excretion is determined solely by glomerular filtration and tubular reabsorption. Evidence of a tubular secretory system was not obtained.