Evidence that both delayed rectifier-type and transient-type k+
currents contribute to the voltage-dependent outward current of the
rat megakaryocyte.
Romero, Elkin, and Richard Sullivan.
Medical Service, Houston VA Medical Center, and the Departments of
Medicine and of Molecular Physiology and Biophysics, Baylor College
of Medicine, Houston, TX 77030
APStracts 3:0321C, 1996.
Megakaryocytes isolated from rat bone marrow express a voltage
-dependent, outward K+ current with complex kinetics of activation and
inactivation. We found that this current could be separated into at
least two components based on differential responses to K+ channel
blockers. One component, which exhibited features of the
"transient" or "A-type" K+ current of excitable
cells, was more strongly blocked by 4-aminopyridine than by
tetrabutylammonium. This current, which we designated as "4-AP
-sensitive," activated rapidly at potentials more positive than
-40 mV and subsequently underwent rapid voltage-dependent
inactivation. A separate current that activated slowly was blocked
much more effectively by tetrabutylammonium than by 4-aminopyridine.
This "TBA-sensitive" component, which resembled a typical
delayed rectifier current, was much more resistant to voltage
-dependent inactivation. The relative contribution of each of these
components varied from cell to cell. The effect of charybdotoxin was
similar to that of 4-aminopyridine. Our data indicate that the
voltage-dependent K+ current of resting megakaryocytes is more
complex than heretofore believed and support the emerging concept
that megakaryocytes possess intricate electrophysiological
properties.
Received 8 April 1996; accepted in final form 7 October 1996.
APS Manuscript Number C193-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996