Elimination of transient secretion of phosphate by alkalinization of plasma in dogs

¹ Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky

Sodium phosphate and creatinine (500 µmoles each) were injected instantaneously into the renal artery of dogs anesthetized with Nembutal. Urine flows of 6–12 ml/min and serum phosphate levels of 3–6 mm/liter were maintained for 1 hr preceding instantaneous injection. Dogs were divided into two major groups, based on steady state conditions imposed: a) systemic acidosis induced by infusion of NaH₂PO₄ and b) systemic alkalosis induced by infusion of Na₂HPO₄ + NaHCO₃. Then, either NaH₂PO₄ or Na₂HPO₄ was injected close-arterially, and the transient excretory response (covering 3–5 min) was studied. The parameter for measuring renal function was the incremental excretion of phosphate per unit injected per one circulation through the kidney. This was compared to the simultaneous and identical parameter for creatinine, considered as a glomerular substance. During systemic acidosis, net transient secretion of phosphate was observed in 73% of the periods after H₂PO₄^– injection, and in 19% of the periods after HPO₄^– injection into renal artery. During systemic alkalosis with formation of alkaline urine, net secretion was observed in 15% of the periods after HPO₄^– injection, and in none of the periods after H₂PO₄^– injection into the renal artery. When paradoxical aciduria occurred during systemic alkalosis, net transient secretion was observed in 30% of the periods after HPO₄^– injection. Data show that the transtubular movement of H₂PO₄^– ion is different from that of HPO_4– ion. The possibility of tubular secretion of H₂PO₄^– ion, as a mechanism of urine acidification, is discussed.

Note:
With the Technical Assistance of Thomas J. Moxley and Robert S. Greathouse