B. Escoubet et al., NONCOORDINATE REGULATION OF EPITHELIAL NA CHANNEL AND NA PUMP SUBUNITMESSENGER-RNAS IN KIDNEY AND COLON BY ALDOSTERONE, American journal of physiology. Cell physiology, 41(5), 1997, pp. 1482-1491
Distal colon and renal cortical collecting ducts are major effecters o
f aldosterone-dependent Na homeostasis. Na is absorbed by entry throug
h an apical amiloride-sensitive Na channel and extruded by Na-K-ATPase
at the basolateral membrane. Using a ribonuclease protection assay, w
e studied, in vivo, aldosterone regulation of alpha-, beta-, gamma-sub
units of the rat epithelial Na channel (rENaC) and alpha(1)- and beta(
1)-subunits of Na-K-ATPase. In the kidney, Na-K-ATPase mRNAs were also
assayed over discrete tubular segments by in situ hybridization. In r
at colon, all three rENaC mRNAs were decreased by adrenalectomy, with
a major effect on beta- and gamma-subunits, and were restored with 7 d
ays, but not 2 days, of aldosterone treatment; in the kidney, however,
only a-transcripts varied. Na-K-ATPase alpha(1)- and beta(1)-subunit
mRNAs in both organs were not (in the case of the beta(1)-subunit) or
were mildly (in the case of the alpha(1)-subunit) affected after adren
alectomy. Our conclusions are as follows: 1) Transcripts of rENaC and
Na-K-ATPase subunits are not coordinately regulated by aldosterone in
vivo; i.e., modulation involves mainly the Na channel, not Na-K-ATPase
; the effect is not of comparable magnitude on each subunit mRNA and d
iffers between tissues. 2) The delay of the aldosterone effect on tran
scripts is much longer than that required to restore normal Na transpo
rt in adrenalectomized rats, indicating that rENaC and Na-K-ATPase sub
unit transcript levels may depend on unidentified early aldosterone-in
duced proteins.