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Volume 272, Number 52, Issue of December 26, 1997
pp. 32919-32924
(Received for publication, April 25, 1997, and in revised form, September 5, 1997)
From INSERM We have examined whether arginine vasopressin
(AVP) can induce a long-term modulation of transepithelial ion
transport in addition to its well known short-term effect. In the
RCCD1 rat cortical collecting duct cell line, an
increase in both short-circuit current and 22Na transport
was observed after several hours of 10
Transcriptional Regulation of Sodium Transport by Vasopressin
in Renal Cells
,
,
,
,
,
,
and
U246 and § U426, Institut
Fédératif de Recherches "Cellules Epithéliales,"
Faculté de Médecine Xavier Bichat, 16, rue Henri Huchard,
75870 Paris Cedex 18, France
8 M AVP
treatment (a concentration above the in vivo physiological range). This delayed effect was partially prevented by apical addition
of 10
5 M amiloride and was blocked by
10
6 M actinomycin D and 2 × 10
6 M cycloheximide. The amounts of mRNA
encoding the
1 (not
1) subunit of
Na+/K+-ATPase and the
and
(not
)
subunits of the amiloride-sensitive epithelial Na+ channel
were significantly increased by AVP treatment. The increase in mRNA
was blocked by actinomycin D, not by amiloride, suggesting a
Na+-independent increase in the rate of transcription of
these subunits. The translation rates of the
1 subunit
of Na+/K+-ATPase and the
and
subunits
of the rat epithelial sodium channel increased significantly, whereas
the translation rates of the other subunits remained unchanged.
Finally, the number of Na+ channels present in the apical
membrane of the cells increased, as demonstrated by enhanced specific
[3H]phenamil binding.
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