Role of intracellular phosphate in the regulation of renal phosphate transport during development

M Barac-Nieto1, H Corey, S M Liu

  • 1Albert Einstein College of Medicine, Department of Pediatrics, Bronx, New York 10461.

Insights

Phosphate transport in kidneys is regulated by factors beyond intracellular phosphate levels. Growth hormone and bone mineralization inhibitors alter phosphate transport without changing intracellular phosphate concentrations.

Area of Science:

  • Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Renal intracellular phosphate concentration ([Pi]i) correlates with age and diet, and inversely with phosphate transport (TRPi).
  • Existing knowledge does not fully explain the high neonatal renal Na(+)-Pi cotransport capacity based solely on [Pi]i.
  • The study investigates if factors other than [Pi]i mediate changes in TRPi due to altered phosphate demand.

Purpose of the Study:

  • To determine if changes in renal tubular phosphate transport (TRPi) are mediated by factors other than intracellular phosphate concentration ([Pi]i).
  • To investigate the role of growth hormone (GH) and bone mineralization inhibition in regulating TRPi.

Main Methods:

  • TRPi measured in vivo; [Pi]i measured in perfused kidneys using nuclear magnetic resonance (NMR).
  • Used genetically growth hormone-deficient dwarf rats and GH-treated rats.
  • Used thyroparathyroidectomized (TPTX) Sprague-Dawley (SD) rats treated with etidronate (EHDP), a bone mineralization inhibitor.

Main Results:

  • GH administration increased TRPi by 38% in dwarf rats without affecting [Pi]i.
  • EHDP administration decreased TRPi by 52% in TPTX SD rats without affecting [Pi]i.
  • Neither GH nor EHDP significantly altered [Pi]i levels.

Conclusions:

  • In rats, alterations in renal tubular phosphate transport (TRPi) in response to changes in phosphate demand occur independently of significant changes in intracellular phosphate concentration ([Pi]i).
  • Growth hormone and inhibition of bone mineralization influence TRPi through mechanisms not directly linked to intracellular phosphate levels.

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