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PMID: 1379590 Published · ppublish English Comparative Study Journal Article Research Support, Non-U.S. Gov't

Expression of the amiloride-blockable Na+ channel by RNA from control versus aldosterone-stimulated tissue.

The Journal of biological chemistry ·Vol. 267 ·No. 23 ·1992-08-15 ·Pages 16061-5

Asher C, Eren R, Kahn L, Yeger O, Garty H

Abstract

The amiloride-blockable Na+ channel was expressed in Xenopus oocytes injected with total RNA isolated from the toad urinary bladder. This system was used to investigate mechanisms that mediate the natriferic action of aldosterone. Incubation of the epithelium with aldosterone for 3 h doubled its channel activity but did not increase the ability of isolated RNA to express functional channels in oocytes. A 20-h incubation with the hormone produced an additional increase of Na+ transport across the intact epithelium and also augmented the channel activity expressed in oocytes by nearly 10-fold. The data are in agreement with our model that aldosterone enhances the apical Na+ permeability of tight epithelia by a short term activation of pre-existing channels, followed by chronic induction of new channel protein. Blocking methyl transfer reactions, previously shown to inhibit the natriferic action of aldosterone in tight epithelia, did not alter the basal or aldosterone-induced response in oocytes.

MeSH Terms
Aldosterone/pharmacology Amiloride/pharmacology Animals Bufo marinus Female Kinetics Oocytes/physiology RNA/genetics,isolation & purification,metabolism Sodium Channels/genetics Urinary Bladder/drug effects,physiology Xenopus laevis
Chemicals
Sodium Channels Aldosterone RNA Amiloride
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Asher C
Department of Membrane Research and Biophysics, Weizmann Institute of Science, Rehovot, Israel.
Eren R
Kahn L
Yeger O
Garty H
Article Info
Journal
The Journal of biological chemistry
Abbr.
J Biol Chem
ISSN
0021-9258
Published
1992-08-15
Pages
16061-5
Language
English
Region
United States
NLM ID
2985121R
Subset
IM
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