Bicarbonate administration to animals and man decreases the renal excretion of calcium. The mechanism of that decrease is a direct renal one, but could be due to either changes in systemic acid-base balance or a direct effect of bicarbonate anion per se. To test the hypothesis that bicarbonate anion per se augments renal calcium absorption, experiments were performed on pentobarbital-anesthetized and thyroparathyroidectomized mongrel dogs with metabolic acidosis. Increased urine bicarbonate was produced by the infusion of L(+)-lysine monohydrochloride, an agent that induces a proximal renal tubular acidosis without changes in glomerular filtration rate when administered intravenously. The infusion of lysine into dogs which did not manifest an increase in urine bicarbonate resulted in no changes in the renal handling of calcium. When urine bicarbonate was increased by lysine infusion, urine calcium excretion declined and absorption increased. This augmentation of calcium absorption occurred despite worsening metabolic acidosis and in the absence of changes in renal sodium handling. When increased sodium excretion occurred with increased bicarbonate excretion in response to lysine infusion, calcium excretion did not fall. We conclude that in the absence of volume expansion the effect of bicarbonate to decrease renal calcium excretion in states characterized by metabolic acidosis is due, at least in part, to changes in urine bicarbonate excretion per se independent of changes in systemic acid-base balance.
|Title of host publication||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Number of pages||5|
|State||Published - Jan 1 1980|
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