To examine the mechanism for the urine-blood PCO 2 gradient in alkaline urine (U-B PCO 2), the authors reevaluated the relationship between U-B PCO 2 and the urinary bicarbonate concentration (UHCO 3 -) during alkali infusion in dogs and rabbits. The results reported in this paper confirm that there is a linear relationship between the U-B PCO 2 and the UHCO 3 - in the dog, but demonstrate that a similar relationship does not occur in the rabbit. These observations in the rabbits cast doubt on the ampholyte hypothesis as an adequate explanation for the U-B PCO 2/UHCO 3 - relationship, because this physicochemical mechanism should produce an invariable elevation of the U-B PCO 2 at high urinary bicarbonate concentrations. Therefore, the authors reevaluated the theoretical basis for this hypothesis. The authors conclude that for the ampholytic effect of bicarbonate to be responsible for the observed relationship between the U-B PCO 2 and UHCO 3 -, bicarbonate ions would have to be secreted into distal nephron tubular fluid that either had no buffering capacity or had a pH half-way between the pK's of the bicarbonate buffer system. Available evidence, however, suggests that urinary bicarbonate is primarily derived from filtered bicarbonate that escapes reabsorption and is concentrated by a fractional reabsorption of water exceeding that of bicarbonate. Therefore, other explanations for the observed linear relationships between the U-B PCO 2 and UHCO 3 - were sought. The most plausible alternatives are stimulation of hydrogen ion secretion by the luminal bicarbonate concentration and the production of a disequilibrium pH by the concentration of bicarbonate and back-diffusion of carbon dioxide.
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