Aldosterone-induced increase in the abundance of na+ channel
subunits.
Asher, Carol, Hanna Wald, Bernard, C. Rossier, and Haim Garty.
Dept. of Membrane Research & Biophysics, The Weizmann Institute
of Science, Rehovot, Israel, 1Nephrology and Hypertension Services,
Hadassah Univ. Hospital, Jerusalem, Israel, and 2Institut de
Pharmacologie et de Toxicologie, Universit[umlaut]a de Lausanne,
Switzerland
APStracts 3:0090C, 1996.
The highly selective, amiloride-blockable Na+ channel is a major
target to the natriferic action of the mineralocorticoid aldosterone.
This channel has been recently cloned from rat colon and is composed
of three homologous subunits denoted a, b, and grENaC (Canessa, et
al. Nature 367: 463, 1994). We have tested the effects of
corticosteroids on the abundance of mRNA coding for each subunit in
kidney cortex and distal colon. Chronic treatment of rats with
aldosterone or dexamethasone, evoked in kidney cortex a small
induction of (rENaC and no change in ( and (rENaC. In distal colon
however, b and grENaC were strongly induced by either aldosterone or
dexamethasone, while arENaC was constitutively expressed. Most of the
aldosterone-induced increase in b and grENaC mRNA, took place during
3-24 hours after elevating plasma aldosterone. A similar differential
induction of rENaC subunits in kidney and colon was also evoked by a
Na+ free diet. The effects of salt deprivation were reversed by
resalinating rats with a t1/2 <2 hours suggesting a high
turnover rate of at least ( and (rENaC. The data are consistent with
the possibility that induction of channel subunits contributes to the
chronic but not the acute response to aldosterone in the colon. Such
a mechanism is not likely to play a major role in cortical collecting
ducts.
Received 17 November 1995; accepted in final form 14 March 1996.
APS Manuscript Number C695-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96