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Articles in PresS, published online ahead of print May 15, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00099.2002
Submitted on March 5, 2002
Accepted on May 13, 2002
1 Physiology, University of Nevada, Reno, NV, USA
2 Physiology, St. Georges Hosptial Medical School, London, United Kingdom
* To whom correspondence should be addressed. E-mail: burt{at}physio.unr.edu.
Ion channels encoded by ether-a-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 if 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 if portal vein myocytes expressed functional ERG channels. Large inward currents with distinctive kinetics were elicited that were inhibited rapidly by E4031 (mean amplitude of the E4031-sensitive current at -120 mV was -205 ± 24 pA; n=14). Deactivation of the E4031-sensitive current was voltage-dependent (mean time constants at -80 mV and -120 mV were 103 ± 9 ms and 33 ± 2 ms, respectively; n=13). Due to the rapid kinetics of mERG currents at more negative potentials there was a substantial non-inactivating '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 E4031. These data show that ERG channels are expressed in murine portal vein myocytes that may contribute to the resting membrane conductance.
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