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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/3465

Title: Rapid activation of K-ATP channels by aldosterone in principal cells of frog skin
Authors: Urbach, V
VAN KERKHOVE, Emmy
Maguire, D
Harvey, BJ
Issue Date: 1996
Publisher: CAMBRIDGE UNIV PRESS
Citation: JOURNAL OF PHYSIOLOGY-LONDON, 491(1). p. 111-120
Abstract: 1. In epithelial cells of frog skin, potassium ions are recycled across the basolateral membrane via an inward-rectifier, ATP-sensitive K+ channel (K-ATP channel). In this study, we show that aldosterone has a stimulatory effect on K-ATP channel activity and we have investigated the involvement of Na+-H+ exchange and intracellular pH (pH(i)) in this phenomenon. 2. Aldosterone (10 nM) produced an increase in the open probability of the K-ATP channel within 15 min from 0.21 +/- 0.05 to 0.93 +/- 0.10 (n = 8), measured in cell-attached patches. Aldosterone also increased the tolbutamide-sensitive K+ current across the basolateral membrane within 30 min from 17.2 +/- 1.9 to 30.3 +/- 1.6 mu A cm(-2) (n = 8) in nystatin-permeabilized whole skins. 3. The K-ATP channel is very sensitive to variations in cytosolic pH within the physiological range 7.0-7.4. 4. The intracellular pH of principal cells is regulated by Na+-H+ exchange, and the stimulatory effect of aldosterone on K-ATP channel activity was abolished by amiloride (100 mu M) added on the basolateral side of the epithelium either before or after aldosterone treatment. 5. We propose that aldosterone activates the K-ATP channels via stimulation of Na+-H+ exchange. The rapidity of aldosterone activation of K-ATP channels is presented as evidence for a novel. non-genomic steroid hormone effect on epithelial ion transport.
Notes: LIMBURGS UNIV CENTRUM,DEPT PHYSIOL,B-3590 DIEPENBEEK,BELGIUM.Urbach, V, NATL UNIV IRELAND UNIV COLL CORK,WELLCOME TRUST CELLULAR PHYSIOL RES UNIT,DEPT PHYSIOL,CORK,IRELAND.
URI: http://hdl.handle.net/1942/3465
Link to publication: http://jp.physoc.org/cgi/content/abstract/491/Pt_1/111
ISI #: A1996TX80400010
ISSN: 0022-3751
Type: Journal Contribution
Appears in Collections: Research publications

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