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Departments of Medicine, Section of Nephrology, and Physiology, Tulane University School of Medicine, and Veterans Affairs Medical Center, New Orleans, Louisiana 70112
The M-1 cell
line, derived from the mouse cortical collecting duct (CCD), is being
used as a mammalian model of the CCD to study
Na+ transport. The present studies
aimed to further define the role of various hormones in affecting
Na+ transport in M-1 cells grown
in defined media. M-1 cells on permeable support, in serum-free media,
developed amiloride-sensitive current 4-5 days after seeding. As
expected for the involvement of epithelial Na+ channels, 
-, 
-, and
-subunits of the epithelial
Na+ channel were identified by
RT-PCR. Either dexamethasone (Dex, 10-100 nM) or aldosterone
(Aldo,
10
6-107
M) for 24 h stimulated transport. Cells grown in the presence of Aldo
and Dex had higher transport than with Dex alone. Spironolactone added
to Dex media decreased transport. The acute effects of hormones reported to inhibit Na+ transport
in CCD were also examined. Epidermal growth factor, phorbol esters, and
increased intracellular Ca2+ with
thapsigargin did not alter transport. Arginine vasopressin caused a
transient increase in transport (probably
Cl secretion), which was
not amiloride sensitive. Also, the protease inhibitor aprotinin
decreased Na+ transport; in
aprotinin-treated cells, trypsin stimulated transport. This study
demonstrates that adrenal steroids (Dex > Aldo) stimulate Na+ transport in M-1 cells. At
least part of this response may represent activation of
mineralocorticoid receptors based on an additive effect of Dex and
Aldo, as well as inhibition by spironolactone. Responses
to immediate-acting hormones is limited. However, an endogenous
protease activity, which activates
Na+ transport, is present in these cells.
aldosterone; dexamethasone; arginine vasopressin; aprotinin; collecting duct cells
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