Hypertonic activation and recovery of system A amino acid transport in renal MDCK cells.
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 gamma-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 repressor protein, leads to increased synthesis of a system A-related protein. The isotonic recovery may require synthesis of new repressor proteins.
Chen
J G
JG
Department of Physiology, Indiana University School of Medicine, Indianapolis 46202-5120, USA.
Coe
M
M
McAteer
J A
JA
Kempson
S A
SA
D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport; D002460:Cell Line; D004285:Dogs; D006977:Hypertension, Renal / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology; D014882:Water-Electrolyte Balance
D000596:Amino Acids