Hypertonie activation and recovery of system a amino acid transport in renal MDCK cells

Jie Guang Chen, Mark Coe, James A. McAteer, Stephen A. Kempson

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20 Scopus citations

Abstract

Amino compounds are abundant within the renal inner medulla, but their possible role during hypertonic stress is not clear. Renal epithelial Madin-Darby canine kidney cells were used to examine the osmoregulation of system A transport, a major Na+-dependent process for neutral amino acid transport. System A activity was markedly increased after 6 h of hypertonic challenge, and intracellular alanine content increased more than twofold. The activation of system A was reversed after 24 h of hypertonic challenge. This downregulation was accompanied by the activation of betaine transport, as measured by -j'-aminobutyric acid uptake. Extracellular betaine prevented the early activation of system A. The hypertonic activation of system A was blocked by actinomycin D and cycloheximide. When cells were returned to isotonic medium after hypertonic activation, the recovery of system A transport also was partially inhibited by actinomycin D and puromycin. The results are consistent with the possibility that hypertonicity, by disrupting a represser protein, leads to increased synthesis of a system A-related protein. The isotonic recovery may require synthesis of new repressor proteins.

Original languageEnglish (US)
Pages (from-to)F419-F424
JournalAmerican Journal of Physiology
Volume270
Issue number3 PART 2
StatePublished - Dec 1 1996

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Keywords

  • Alanine
  • Betaine
  • Carbon-14-labeled u-methylaminoisobutyric acid
  • Kidney
  • Madin-darby canine kidney cells
  • Osmoregulation

ASJC Scopus subject areas

  • Physiology (medical)
  • Physiology

Cite this

Chen, J. G., Coe, M., McAteer, J. A., & Kempson, S. A. (1996). Hypertonie activation and recovery of system a amino acid transport in renal MDCK cells. American Journal of Physiology, 270(3 PART 2), F419-F424.