Magnesium shifts the voltage dependence of activation of the
delayed rectifier potassium current in guinea pig ventricular
myocytes.
Williams, Beatrice A., Gregory N. Beatch.
Bureau of Drug Research, Drugs Directorate, Health Protection
Branch, Health Canada, Ottawa, Ontario, Canada, K1A 0L2 and Division
of Cardiology, University of Ottawa Heart Institute, Faculty of
Medicine, University of Ottawa, Ottawa, Ontario, Canada, K1Y 4E9
APStracts 3:0491H, 1996.
The sensitivity of the delayed-rectifier K+-current (IK) to
intracellular Mg2+ was investigated in guinea pig ventricular
myocytes using the whole-cell patch-clamp technique. An increase in
free [Mg2+]i led to a dose-dependent decrease in IK with half-maximal
effect of approximately 20nM. Activation of IK was shifted towards
more positive voltages on increasing [Mg2+]i, but little effect was
observed on activation and deactivation kinetics. Isoproterenol
increased IK, and was partially reversible, in both control and 100nM
[Mg2+]i. The antiarrhythmic drug, dofetilide, was used to separate IK
into its two components, IKr and IKs. The magnitude of both
components decreased to a similar extent with an increase in [Mg2+]i.
As [Mg2+]i was reduced, however, the number of experiments in which
the dofetilide-sensitive current, IKr, displayed inward rectification
was reduced. In contrast to results previously reported for frog
myocytes, it is unlikely that Mg2+ effects on guinea pig IK are
mediated by a protein phosphatase.
Received 17 November 1997; accepted in final form 9 October 1996.
APS Manuscript Number H1082-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996