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Voltage-dependent K+ currents in smooth muscle cells from mouse gallbladder.

Jaggar J, Mawe G, Nelson MT

American Journal of Physiology-Gastrointestinal and Liver Physiology. 1998;274( 4 Pt 1):G687-93.

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Abstract

The ionic mechanisms associated with the control of gallbladder contractility are incompletely understood. One type of K+ current, the voltage-dependent K+ (KV) current, is relatively uncharacterized in gallbladder cells and may contribute to muscular excitability. The main focus of this study was therefore to determine the voltage dependence and pharmacological nature of this K+ current in isolated myocytes from mouse gallbladder, using the patch-clamp technique. Currents through Ca(2+)-activated K+ channels were minimized by buffering of intracellular Ca2+ (20 nM free Ca2+) and by inclusion of 1 mM tetraethylammonium (TEA+) in the bathing solution. With 140 mM symmetrical K+, membrane depolarization increased K+ currents, independent of driving force, as assessed by tail current analysis. Half-maximal activation of K+ currents occurred at approximately 1 mV and increased e-fold per 9 mV. Inactivation also increased on depolarization, with a midpoint of -24 mV. Single KV channels were recorded in the cell-attached configuration, exhibiting a single-channel conductance of 4.9 pS. TEA+ at 10 mM reduced KV currents by 36%. At +50 mV, 1 mM and 10 mM 4-aminopyridine inhibited currents by 18% and 35%, respectively, whereas 1 and 10 mM 3,4-diaminopyridine inhibited currents by 11% and 21%, respectively. Quinine inhibited KV currents (at +50 mV, 100 microM and 1 mM quinine inhibited current by 24% and 70%, respectively). In summary, we describe voltage-activated K+ currents from the mouse gallbladder that are likely to contribute to the control of muscular excitability.

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UNITED STATES
Volume:
274( 4 Pt 1)
Start page:
G687
End page:
93
Pagination:
G687-93
Access state:
Active

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Manchester eScholar ID:
uk-ac-man-scw:1d16416
Created:
30th August, 2009, 13:57:01
Last modified:
3rd March, 2010, 17:07:53

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