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1 Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557-0046; and 2 Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, SW17 0RE London, United Kingdom
Ion channels encoded by
ether-à-go-go-related genes (ERG) have been implicated
in repolarization of the cardiac action potential and also as
components of the resting membrane conductance in various cells. The
aim of the present study was to determine whether ERG channels were
expressed in smooth muscle cells isolated from portal vein. RT-PCR
demonstrated the expression of murine ERG (mERG), and real-time
quantitative PCR showed that the mERG1b isoform predominated over the
mERG1a, mERG2, and mERG3 in portal vein. Single myocytes from portal
vein displayed membrane staining with an ERG1-specific antibody. Whole
cell voltage-clamp experiments were performed to determine whether
portal vein myocytes expressed functional ERG channels. Large inward
currents with distinctive kinetics were elicited that were inhibited
rapidly by E-4031 (mean amplitude of the E-4031-sensitive current at
120 mV was 205 ± 24 pA; n = 14). Deactivation
of the E-4031-sensitive current was voltage dependent (mean time
constants at 80 and 120 mV were 103 ± 9 and 33 ± 2 ms,
respectively; n = 13). Because of the rapid kinetics of
mERG currents at more negative potentials, there was a substantial
noninactivating "window" current that reached a maximum of
66 ± 10 pA at 70 mV. Complete portal veins exhibited
spontaneous contractile activity in isometric tension experiments, and
this activity was modified significantly by E-4031. These data show
that ERG channels are expressed in murine portal vein myocytes that may
contribute to the resting membrane conductance.
vascular smooth muscle; ether-à-go-go-related genes; potassium channel
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