Hypertonic activation and recovery of system a amino acid transport
in renal mdck cells.
Chen, Jie-Guang, Mark Coe, James A. McAteer, and Stephen A. Kempson.
Departments of Physiology & Biophysics, and Anatomy, Indiana
University School of Medicine, Indianapolis, IN 46202-5120
APStracts 2:0163F, 1995.
Amino compounds are abundant within the renal inner medulla but their
possible role during hypertonic stress is not clear. Renal epithelial
MDCK 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 2-fold. 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.
Received 8 May 1995; accepted in final form 11 September 1995.
APS Manuscript Number F151-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 31 October 95