Jg. Chen et al., HYPERTONIC ACTIVATION AND RECOVERY OF SYSTEM-A AMINO-ACID-TRANSPORT IN RENAL MDCK CELLS, American journal of physiology. Renal, fluid and electrolyte physiology, 39(3), 1996, pp. 419-424
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 osmoregulati
on of system A transport, a major Na+-dependent process for neutral am
ino 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 ac
tivation 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 par
tially inhibited by actinomycin D and puromycin. The results are consi
stent with the possibility that hypertonicity, by disrupting a repress
or protein, leads to increased synthesis of a system A-related protein
. The isotonic recovery may require synthesis of new repressor protein
s.