Relationship between Phosphaturia and Acute Hypercapnia in the Rat

Abstract

Standard clearance studies were performed in mechanically ventilated intact and acutely thyroparathyroidectomized (TPTX) rats to document and characterize the effect of hypercapnia (HC) on urinary phosphorus excretion (U_PV). HC as compared to normocapnia (NC) was associated with an increase in U_PV in intact (62.5 vs. 7.93 μg/min) and TPTX (30.5 vs. 0.59 μg/min) rats, an increase in filtered load of phosphorus in intact (218 vs. 191 μg/min) and TPTX (243 vs. 146 μg/min) rats, an increase in blood bicarbonate concentration in intact (27.8 vs. 26.0 meq/liter) and TPTX (24.5 vs. 22.3 meq/liter) animals, and a decrease in blood pH in intact (7.15 vs. 7.42) and TPTX (7.07 vs. 7.39) rats. Additional TPTX rats with NC and HC were studied during phosphorus infusion at a comparable filtered load of phosphorus (NC = 307 μg/min and HC = 328 μg/min). U_PV was 18.5 μg/min in NC and 85.2 μg/min in HC animals. Intact NC animals infused with NaHCO₃ achieved a blood bicarbonate of 45.9 meq/liter compared to 26.0 meq/liter in intact NC NaCl-infused rats. U_PV was 10.0 μg/min in the NaHCO₃ and 7.93 μg/min in NaCl-infused animals. In intact HC animals infused with NaHCO₃, blood pH was 7.36 compared to 7.42 in NC intact NaCl-infused animals. U_PV was 83.2 μg/min in the HC bicarbonate-infused and 7.93 μg/min in the NC NaCl-infused rats. These experiments demonstrate that elevated blood carbon dioxide tension per se increases U_PV. Increases in filtered load of phosphorus and blood bicarbonate which are associated with HC contribute to the phosphaturia as does parathyroid hormone. The phosphaturia is not dependent upon reduction of extracellular pH.