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First published online 1 September 2005
doi: 10.1242/jcs.02540

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Sulphonylurea receptors differently modulate ICC pacemaker Ca²⁺ activity and smooth muscle contractility

¹ Department of Cell Physiology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
² Department of Physiological Medicine,Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
³ Department of Anatomy and Cell Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan
⁴ Department of Molecular and Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya 467-8603, Japan
⁵ Department of Internal Medicine, Aichi-Gakuin University School of Dentistry, Nagoya 464-8651, Japan
⁶ Biochemical Engineering of Environment Center, Faculty of Chemical Science and Engineering, University of Petroleum, Beijing 102249, China
⁷ Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK

^* Author for correspondence (e-mail: h44673a{at}nucc.cc.nagoya-u.ac.jp)

Accepted 13 June 2005

Appropriate gastrointestinal motility is essential to properly control the body energy level. Intracellular Ca²⁺ ([Ca²⁺]_i) oscillations in interstitial cells of Cajal (ICCs; identified with c-Kit immunoreactivity) are considered to be the primary mechanism for the pacemaker activity in gastrointestinal motility. In the present study, RT-PCR examinations revealed predominant expression of the type 1 isoform of sulphonylurea receptors (SUR1) in ICCs of the mouse ileum, but expression of SUR2 was predominant in smooth muscle. In cell clusters prepared from the same tissue, smooth muscle contractility and pacemaker [Ca²⁺]_i activity in ICCs were found to be differentially modulated by K_ATP channel openers and sulphonylurea compounds, in accordance with the expression of SUR isoforms. 1 µM cromakalim nearly fully suppressed the mechanical activity in smooth muscle, whereas ICC pacemaker [Ca²⁺]_i oscillations persisted. Greater concentrations (10 µM) of cromakalim attenuated pacemaker [Ca²⁺]_i oscillations. This effect was not reversed by changing the reversal potential of K⁺, but was prevented by glibenclamide. Diazoxide at 30 µM terminated ICC pacemaker [Ca²⁺]_i oscillations, but again treatment with high extracellular K⁺ did not restore them. These results suggest that SUR can modulate pacemaker [Ca²⁺]_i oscillations via voltage-independent mechanism(s), and also that intestinal pacemaking and glucose control are closely associated with SUR.

Key words: Gastrointestinal motility, Pacemaker, Intracellular Ca²⁺ oscillations, Sulphonylurea receptors, c-Kit immunoreactivity, K⁺ channel openers

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