AJP - Cell Physiology, Vol 263, Issue 4 C825-C837, Copyright © 1992 by American Physiological Society
Aldosterone alters the open probability of amiloride-blockable sodium channels in A6 epithelia
A. E. Kemendy, T. R. Kleyman and D. C. Eaton
Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322.
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.
