Aldosterone alters the open probability of amiloride-blockable sodium channels in A6 epithelia
- 1 October 1992
- journal article
- Published by American Physiological Society in American Journal of Physiology-Cell Physiology
- Vol. 263 (4), C825-C837
- https://doi.org/10.1152/ajpcell.1992.263.4.c825
Abstract
We used patch-clamp methods to examine the effects of depletion and readdition of aldosterone on single, highly selective, amiloride-blockable sodium channels in the A6 cell line. Single-channel characteristics changed little before 24 h of continuous aldosterone depletion, although there was some reduction in short-circuit current. Thereafter, apical sodium permeability, measured as product of channel number per patch and individual channel open probability (NPo), was reduced between five- and sevenfold, primarily due to a large decrease in channel mean open time. With about the same time course, short-circuit current also decreased approximately fivefold. Readdition of aldosterone to depleted cells produced an increase in NPo within 2 h, primarily through an increase in mean open time. After readdition, channel number per patch increased twofold compared with cells not hormone deprived, with a return to control levels between 24 and 48 h after continuous exposure. The increase in short-circuit current followed a similar time course. The primary effect of aldosterone appears to be modulation of the open time of channels continuously present in the apical membrane, rather than promotion of the appearance or disappearance of channels from the membrane. In particular, it cannot be demonstrated statistically that aldosterone removal reduces the number of channels per patch, and there may actually be up to a twofold increase after a long period of aldosterone depletion.Keywords
This publication has 8 references indexed in Scilit:
- Blocker-related changes of channel density. Analysis of a three-state model for apical Na channels of frog skin.The Journal of general physiology, 1990
- Amiloride-sensitive Na channels from the apical membrane of the rat cortical collecting tubule.Proceedings of the National Academy of Sciences, 1986
- Amiloride-sensitive trypsinization of apical sodium channels. Analysis of hormonal regulation of sodium transport in toad bladder.The Journal of general physiology, 1983
- Aldosterone control of the density of sodium channels in the toad urinary bladderThe Journal of Membrane Biology, 1982
- The role of sodium-channel density in the natriferic response of the toad urinary bladder to an antidiuretic hormoneThe Journal of Membrane Biology, 1982
- Current-voltage analysis of apical sodium transport in toad urinary bladder: Effects of inhibitors of transport and metabolismThe Journal of Membrane Biology, 1980
- Site of Action of Aldosterone on the Bladder of the ToadNature, 1963