Identification and characteristics of the delayed rectifier k+
current in fetal mouse ventricular myocytes.
Wang, L., and H. J. Duff.
Department of Medicine, University of Calgary, Calgary, Alberta,
Canada
APStracts 3:0106H, 1996.
Although the genetics of mammalian cardiac K+ channels have been most
intensively investigated in mouse, there are limited data available
from the electrophysiological studies of the K+ currents in native
mouse cardiac myocytes, especially in fetal mouse heart. The present
study utilized whole-cell patch clamp techniques to assess the
delayed rectifier K+ current (IK) in fetal (18th day of gestation)
mouse ventricular myocytes. IK in fetal mouse ventricular myocytes
activated rapidly, displayed a negative slope conductance of the
current-voltage relationships at test potentials > 0 mV,
satisfied the envelope of IK-tail test for a single component and was
very sensitive to dofetilide. These characteristics confirm that this
current is the rapidly activating component of IK known as IKr. In
addition, dofetilide dramatically prolonged action potential duration
in single ventricular myocytes as well as in ventricular myocardium,
suggesting that IKr plays a dominant role in action potential
repolarization in fetal mouse heart. From these data we can conclude
that this is the first demonstration that the native fetal mouse
cardiac myocytes express IKr, which functions as a dominant
repolarizing K+ current.
Received 9 August 1995; accepted in final form 7 November 1995.
APS Manuscript Number H748-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96