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 HPO4– ion. The possibility of tubular secretion of H2PO4– ion, as a mechanism of urine acidification, is discussed.
MP007FUROSEMIDE DOES NOT CAUSE ENAC-INDEPENDENT URINE ACIDIFICATION IN MAN
