Reconstitution of a K(ATP) channel from basolateral membranes of
Necturus enterocytes.
Mayorga-Wark, O., W. P. Dubinsky, and Stanley G. Schultz.
Department of Physiology and Cell Biology, University of Texas
Medical School at Houston
APStracts 2:0123C, 1995.
We have previously reported that basolateral membrane vesicles
isolated from Necturus small intestinal epithelial cells and
incorporated into planar phospholipid bilayers display a highly
selective "maxi" conductance K+ channel whose open-time
probability is affected by voltage. We now report that this channel
is inhibited by MgATP in the solution bathing the intracellular face
of the channel but not by Mg2+ or the Na+ or K+ salts of ATP; the
effects of MgATP can be prevented or reversed by MgADP. The channel
is also inhibited by the nonhydrolyzable ATP analogue MgATP-[gamma]-S
and the sulfonylurea derivatives tolbutamide and glibenclamide; all
of these agents are effective in the intracellular compartment but
not when added to the extracellular compartment alone. Channel
activity is stimulated by the "K+ channel opener", diazoxide,
which also reverses the effect of glibenclamide but not of MgATP. The
possible role of this channel as a mediator of the parallelism
between basolateral membrane Na+-K+ pump activity and the macroscopic
K+ conductance of that barrier is discussed.
Received 21 November 1994; accepted in final form 13 February
1995.
APS Manuscript Number C684-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.