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Am J Physiol Gastrointest Liver Physiol 284: G392-G398, 2003. First published November 13, 2002; doi:10.1152/ajpgi.00325.2002
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Vol. 284, Issue 3, G392-G398, March 2003

ERG K+ channels modulate the electrical and contractile activities of gallbladder smooth muscle

Edward Parr1, Maria J. Pozo2, Burton Horowitz3, Mark T. Nelson4, and Gary M. Mawe1,4

Departments of 1 Anatomy and Neurobiology and 4 Pharmacology, The University of Vermont, Burlington, Vermont 05405; 2 Department of Physiology, University of Extremadura, 10071 Cáceres, Spain; and 3 Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada 89557

The current study was undertaken to test the existence and possible role of ether-a-go-go-related gene 1 (ERG1) protein 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 E-4031 (100 nM-1 µM) or cisapride (100 nM-2 µM) caused concentration-dependent excitation of guinea pig GBSM that was not affected by 500 nM TTX + 5 µM atropine, and E-4031 also depolarized the resting membrane potential. In muscle strip studies, E-4031 either induced phasic contractions or significantly increased the amplitude of phasic contractions in spontaneously active tissues (P = 0.001). E-4031 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.

biliary motility; rapidly activated delayed rectifier; E-4031; cisapride


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