Phenylephrine suppresses outward k+ currents in rat atrial
myocytes.
Wagoner, David R. Van, Margaret Kirian, and Michelle Lamorgese.
Department of Molecular Cardiology, Research Institute, The
Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195
-5069
APStracts 3:0090H, 1996.
The modulation of whole cell K+ currents by the [alpha]1-adrenergic
agonist, phenylephrine, was studied in isolated rat atrial myocytes,
using perforated patch whole cell recording techniques. The outward
K+ current in these myocytes consists of two inactivating components
(iKf and iKs) which differ in the kinetics of inactivation and
recovery from inactivation, and a non-inactivating component, (iKss).
Superfusion of these myocytes with 10 [mu]M phenylephrine caused a
rapid suppression of iKss, with little effect on the other current
components. This effect of phenylephrine could be mimicked by
exogenous application of 1,2-dioctanoylglycerol?(20 [mu]M), a
membrane permeant diacylglycerol analog; however, it was clearly
distinct from the effect of 5?nM [alpha]- dendrotoxin, which
selectively suppressed the slowly-inactivating current component,
iKs, while having no effect on iKss. At a dose of 50 [mu]M,
phenylephrine also suppressed iKs. There was no significant effect of
phenylephrine (10 or 50 [mu]M), or [alpha]-dendrotoxin (5 nM) on the
rapidly-inactivating current component, iKf. The kinetic and
pharmacological differences between these current components suggest
that they represent the activity of distinct K+ channels.
Received 14 July 1995; accepted in final form 16 February 1996.
APS Manuscript Number H655-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96