Our previous studies showed that the phosphaturic effect of parathyroid hormone (PTH) is blunted during acute-phase endotoxemia in anesthetized rats. However, the possibility that the antiphosphaturia was secondary to hyponatriuresis due to endotoxin (Et)-induced acute renal failure could not be ruled out. The objective of this study was to evaluate phosphate (Pi) excretion during early- and late-phase endotoxemia in conscious rats fed by total parenteral nutrition. Male Wistar rats weighing 270 g were used. Urine samples were taken to determine the Pi excretion rate for 12 h just after Et (E. coli B055) challenge (early-phase endotoxemia), and for 12 h after a 36-h recovery period following Et challenge (late-phase endotoxemia). Rats given isovolumetric saline instead of Et served as controls. Et injection reduced endogenous creatinine clearance markedly (0.88 +/- 0.12 ml/min, P < 0.0001, n = 7) and caused hyponatriuresis (0.80 +/- 0.19 microliters/min, P < 0.001) compared with saline injection (1.78 +/- 0.10 ml/min and 3.12 +/- 0.39 microliters/min, respectively, n = 8) during the early phase. Greater phosphaturia and hypocalciuria were observed simultaneously during early- (Pi excretion = 4.18 +/- 1.38 micrograms/min, P < 0.05; calcium excretion = 0.70 +/- 0.14 micrograms/min, P < 0.05) and late-phase (4.76 +/- 1.72 micrograms/min, P < 0.05; 0.60 +/- 0.18 micrograms/min, P < 0.05, respectively) endotoxemia (n = 8) in comparison with the respective control values (1.61 +/- 0.39 and 1.40 +/- 0.21 micrograms/min, early; 0.34 +/- 0.14 and 1.97 +/- 0.55 micrograms/min, late, n = 6). Et adminidstration resulted in a significantly increased plasma PTH concentration during the late phase (34.7 +/- 7.0 pg/ml, P < 0.05) compared with saline administration (15.4 +/- 2.4 pg/ml). In conclusion, these data suggest that the hyperphosphaturia during endotoxemia lasting longer than 12 h is attributable to elevated PTH secretion.