title: Parathyroid hormone activity increases during endotoxemia in conscious rats.
abstract: 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.
authors.affiliation: Third Department of Surgery, University of Tokyo.
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: Y
authors.initials: Y
authors.lastname: Mimura
authors.forename: K
authors.initials: K
authors.lastname: Uno
authors.forename: M
authors.initials: M
authors.lastname: Yamakawa
mesh_terms: D000818:Animals; D001639:Bicarbonates / Q000652:urine; D002245:Carbon Dioxide / Q000097:blood; D002395:Catecholamines / Q000652:urine; D003404:Creatinine / Q000652:urine; D019446:Endotoxemia / Q000378:metabolism*; D004731:Endotoxins / Q000633:toxicity; D007668:Kidney / Q000187:drug effects; D008297:Male; D010280:Parathyroid Glands; D010281:Parathyroid Hormone / Q000097:blood*; D010288:Parenteral Nutrition; D010710:Phosphates / Q000652:urine; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000652:urine; D014556:Urine / Q000737:chemistry
chemical_list: D001639:Bicarbonates; D002395:Catecholamines; D004731:Endotoxins; D010281:Parathyroid Hormone; D010710:Phosphates; D002245:Carbon Dioxide; C044101:endotoxin, Escherichia coli; D012964:Sodium; D003404:Creatinine