Citrate excretion during intrarenal arterial precursor infusion in the alkalotic dog

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Abstract
The mechanism of citrate excretion was studied in alkalotic dogs by the stop-flow technique during intrarenal arterial infusion of labeled Krebs cycle precursors. When succinate-14C was infused, citrate in stop-flow samples showed a reabsorptive minimum in the proximal area, but the specific activity of the citrate (SAcit) in this same area showed a significant peak. The increased SAcit was not related to the reabsorption of citrate. Intravenous citrate infusion did not influence this pattern. The same stop-flow pattern was obtained with infusion of malate-14C. However, the peak of SAcit was abolished when the blood malate level was elevated by intravenous infusion of the acid. Benemid did not alter the citrate patterns in stop-flow samples. These observations indicate that both the tubular reabsorption of citrate and the tubular synthesis and secretion of citrate from precursors are localized in the proximal tubule. The secretory mechanism is inhibited by malate, but it is independent of PAH [para-amino hippurate] secretion. In another series of experiments with malonate using the isotopic split renal function technique, it was found that 10-16% of the citrate excreted during malonate infusion is derived from the malonate itself.

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