Effects of Alkalosis on Plasma Concentration and Urinary Excretion of Inorganic Phosphate in Man.

In 1924, Haldane, Wigglesworth, and Wood-row reported on the effect of reaction changes on human inorganic metabolism (1). They found that respiratory alkalosis caused a sharp fall and respiratory acidosis a sharp rise in serum phosphorus concentration. They also examined metabolic changes induced by oral ingestion of Na-HCO3 or NH4Cl for several days, but respiratory compensation would have minimized pH changes under the conditions of their experiments. They found no significant deviation of serum phosphorus from normal values. The influence of alkalosis on serum and urinary phosphorus has been intermittently observed since that time during experiments on hydrogen ion disturbances in dogs and in man (2-9). However, most recent reviews on phosphorus metabolism and the para-thyroids do not mention the effect of blood hydrogen ion concentration or carbon dioxide tension upon the concentration of phosphorus in the serum or upon the urinary excretion and clearance of phosphorus (10-22). Our study was undertaken to evaluate the range of variation of plasma phosphorus concentration under the influence of elevated blood pH, to ascertain whether hydrogen ion concentration or CO2 content is the critical determinant, and to consider possible explanations for the fall in concentration of phosphorus. Methods Sixteen experiments were performed between 8 a.m. and 2 p.m. in eleven healthy young adults from 20 to 40 years of age. Three major experimental designs were used. In six experiments respiratory alkalosis was induced by voluntary hyperventilation. The Pco2 of expired air was monitored with a continuous infrared CO2 analyzer. Breathing was controlled to reduce the end-expiratory Pco2 from a control range of 35 to 40 mm Hg to a range of 13 to 20 mm Hg. In four experiments hyperventilation without alka-losis was studied as a control. Two of these were conducted with a Bird Mark VIII respirator using both positive and negative pressures. After a control period of selfregulated respiration, hyperventilation was induced by increase in rate and depth of exchange. The inspired gas mixture was adj usted to contain sufficient CO2 to maintain end-expiratory Pco2 at control levels. After stabilization under these conditions, CO2 was removed from the inspired gas mixture, and respiratory alkalosis was induced. In two further experiments voluntary active hyperventilation was carried out in a tent receiving 10%o CO2 and 90% 02 so that end-expiratory Pco2 was maintained at control levels. In six other experiments, metabolic alkalosis was induced. NaHCO2, in amounts from 3.5 to 4.5 mEq per …