Membrane potential in smooth muscle cells from hypertrophic rat portal vein

1983 ◽  
Vol 39 (11) ◽  
pp. 1288-1290 ◽  
Author(s):  
S. B. Sigurdsson ◽  
B. Uvelius
2007 ◽  
Vol 292 (1) ◽  
pp. C468-C476 ◽  
Author(s):  
Shuk Yin M. Yeung ◽  
Iain A. Greenwood

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.


1992 ◽  
Vol 456 (1) ◽  
pp. 541-556 ◽  
Author(s):  
P Pacaud ◽  
G Loirand ◽  
T B Bolton ◽  
C Mironneau ◽  
J Mironneau

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