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Articles in PresS, published online ahead of print November 13, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00325.2002
Submitted on August 6, 2002
Accepted on October 30, 2002
1 Department of Anatomy and Neurobiology, The University of Vermont, Burlington, VT, USA
2 Department of Physiology, University of Extremadura, Caceres, Extremadura, Spain
3 Department of Physiology and Cell Biology, Unversity of Nevada School of Medicine, Reno, NV, USA
4 Department of Pharmacology, The University of Vermont, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: gmawe{at}zoo.uvm.edu.
The current study was undertaken to test the existence and possible role of ERG1 K+ channels in gallbladder smooth muscle (GBSM). Transcripts encoding ERG1 were detected in human, mouse and guinea pig GBSM, and ERG1 immunoreactivity was observed in GBSM cells. In intracellular voltage recordings, addition of E4031 (100nM-1µM) or cisapride (100nM-2µM) caused concentration-dependent excitation of guinea pig GBSM that was not affected by 500nM TTX plus 5µM atropine, and E4031 also depolarized the resting membrane potential. In muscle strip studies, E4031 either induced phasic contractions or significantly increased the amplitude of phasic contractions in spontaneously active tissues (P=0.001). E4031 also potentiated bethanechol-induced contractions. In conclusion, ERG1 channels are expressed in the GBSM where they play a role in excitation-contraction coupling, probably by contributing to repolarization of the plateau phase of the action potential and to the resting membrane potential.
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