Hyperosmotic stress up-regulates amino acid transport in vascular endothelial cells

Stephen A. Kempson, Martha J. Hoshaw, Rose S. Hinesley, James A. Mcateer

Research output: Contribution to journalArticle

9 Scopus citations


Cultured vascular endothelial cells take up L-proline by sodium- dependent transport. Cells incubated in medium made hyperosmotic by addition of sucrose showed a dose-dependent increase in Na+/proline cotransport. Studies with α-(methylamino)isobutyric acid revealed that the up-regulation was specific for amino acid transport system A. Up-regulation was blocked by actinomycin D and cycloheximide, indicating roles for gene transcription and protein synthesis. Upregulation was maximum after five to six hours of hyperosmotic treatment, but returned to control levels when osmotic stress was maintained for 24 hours. The decline at 24 hours was accompanied by a significant increase in Na+/γ-aminobutyric acid cotransport. The activity of this system, which also transports betaine, remained unchanged after just five hours of hyperosmotic stress. Inclusion of betaine in the hyperosmotic medium reduced up-regulation of system A. Na/Pi cotransport also was upregulated by five hours of hyperosmotic stress. Up-regulation of system A, but not Na/Pi cotransport, was detected in isolated membrane fractions indicating that increased activity of this membrane transport system may be one mechanism by which vascular endothelial cells accumulate amine acids. The amine acids may act as organic osmolytes to help maintain normal cell volume during the early phase of hyperosmotic stress.

Original languageEnglish (US)
Pages (from-to)1332-1339
Number of pages8
JournalKidney international
Issue number5
StatePublished - Jan 1 1997


  • Amino acids
  • Endothelial cells
  • Hyperosmotic stress
  • Membrane transport
  • Phosphate
  • System A
  • Transport
  • Volume

ASJC Scopus subject areas

  • Nephrology

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    Kempson, S. A., Hoshaw, M. J., Hinesley, R. S., & Mcateer, J. A. (1997). Hyperosmotic stress up-regulates amino acid transport in vascular endothelial cells. Kidney international, 52(5), 1332-1339. https://doi.org/10.1038/ki.1997.458