Am J Physiol Cell Physiol AJP: Endocrinology and Metabolism
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Am J Physiol Cell Physiol 292: C468-C476, 2007. First published July 26, 2006; doi:10.1152/ajpcell.00142.2006 Free Article
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VASCULAR BIOLOGY

Pharmacological and biophysical isolation of K+ currents encoded by ether-à-go-go-related genes in murine hepatic portal vein smooth muscle cells

Shuk Yin M. Yeung and Iain A. Greenwood

Division of Basic Medical Sciences, Ion Channels and Cell Signalling Research Centre, St. George's, University of London, London, United Kingdom

Submitted 30 March 2006 ; accepted in final form 25 July 2006

Previous studies have shown that murine portal vein myocytes express ether-à-go-go related genes (ERGs) and exhibit distinctive currents when recorded under symmetrical K+ conditions. The aim of the present study was to characterize ERG channel currents evoked from a negative holding potential under conditions more pertinent to a physiological scenario to assess the possible functional impact of this conductance. Currents were recorded with ruptured or perforated patch variants of the whole cell technique from a holding potential of –60 mV. Application of three structurally distinct and selective ERG channel blockers, E-4031, dofetilide, and the peptide toxin BeKM-1, all inhibited a significant proportion of the outward current and abolished inward currents with distinctive "hooked" kinetics recorded on repolarization. Dofetilide-sensitive currents at negative potentials evoked by depolarization to +40 mV had a voltage-dependent time to peak and rate of decay characteristic of ERG channels. Application of the novel ERG channel activator PD-118057 (1–10 µM) markedly enhanced the hooked inward currents evoked by membrane depolarization and hyperpolarized the resting membrane potential recorded by current clamp and the perforated patch configuration by ~20 mV. In contrast, ERG channel blockade by dofetilide (1 µM) depolarized the resting membrane potential by ~8 mV. These data are the first record of ERG channel currents in smooth muscle cells under quasi-physiological conditions that suggest that ERG channels contribute to the resting membrane potential in these cells.

vascular smooth muscle; voltage-dependent K+ current; membrane excitability


Address for reprint requests and other correspondence: I. A. Greenwood, Div. of Basic Medical Sciences, Ion Channels and Cell Signalling Research Centre, St. George's, Univ. of London, London SW17 0RE, UK (e-mail: i.greenwood{at}sgul.ac.uk)






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