Recovery of renal tubule phosphate reabsorption despite reduced levels of sodium-phosphate transporter.

BACKGROUND The acute effect of parathyroid hormone (PTH) on phosphate transport has been reported to be mediated by rapid downregulation of sodium-phosphate transporter (NaPi-IIa) protein, but the association was observed with pharmacological doses of PTH. OBJECTIVE To explore the effects of physiological doses of PTH on NaPi-IIa protein and its relationship to phosphate transport. METHODS Acute clearance studies were performed in parathyroidectomized rats given a bolus i.v. physiological dose (1 microg) of bovine PTH(1-34) and NaPi-IIa protein concentrations were examined at different time intervals. RESULTS Fractional excretion of phosphate increased from 0.031+/-0.006 (mean+/-S.E.) to 0.238+/-0.059 (P<0.01 compared with baseline and compared with controls) at 40 min and returned to control values by 120 min. Urinary cAMP concentrations were increased at 20 min only. Superficial cortex brush-border membrane (BBM) NaPi-IIa protein was decreased from baseline at both 40 and 120 min (P<0.01) and did not recover at 240 min (P<0.01 compared with baseline and compared with controls). CONCLUSION These results confirm that PTH, even in physiological dosage, causes a rapid decrease in BBM NaPi-IIa, but subsequent recovery of phosphate reabsorption is poorly correlated with BBM concentrations of NaPi-IIa protein. This suggests that transport mechanisms other than NaPi-IIa are important in renal phosphate reabsorption.