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Am J Physiol Cell Physiol 291: C1405-C1411, 2006. First published July 5, 2006; doi:10.1152/ajpcell.00519.2005
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RECEPTORS AND SIGNAL TRANSDUCTION

Involvement of stretch-activated cation channels in hypotonically induced insulin secretion in rat pancreatic beta-cells

Miki Takii, Tomohisa Ishikawa, Hidetaka Tsuda, Kazumitsu Kanatani, Takaaki Sunouchi, Yukiko Kaneko, and Koichi Nakayama

Department of Cellular and Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka City, Shizuoka, Japan

Submitted 17 October 2005 ; accepted in final form 22 June 2006

In isolated rat pancreatic beta-cells, hypotonic stimulation elicited an increase in cytosolic Ca2+ concentration ([Ca2+]c) at 2.8 mM glucose. The hypotonically induced [Ca2+]c elevation was significantly suppressed by nicardipine, a voltage-dependent Ca2+ channel blocker, and by Gd3+, amiloride, 2-aminoethoxydiphenylborate, and ruthenium red, all cation channel blockers. In contrast, the [Ca2+]c elevation was not inhibited by suramin, a P2 purinoceptor antagonist. Whole cell patch-clamp analyses showed that hypotonic stimulation induced membrane depolarization of beta-cells and produced outwardly rectifying cation currents; Gd3+ inhibited both responses. Hypotonic stimulation also increased insulin secretion from isolated rat islets, and Gd3+ significantly suppressed this secretion. Together, these results suggest that osmotic cell swelling activates cation channels in rat pancreatic beta-cells, thereby causing membrane depolarization and subsequent activation of voltage-dependent Ca2+ channels and thus elevating insulin secretion.

calcium ion; swelling; patch-clamp; gadolinium


Address for reprint requests and other correspondence: T. Ishikawa, Dept. of Cellular and Molecular Pharmacology, Graduate School of Pharmaceut. Sci., Univ. of Shizuoka, 52-1 Yada, Suruga-Ku, Shizuoka City, Shizuoka 422-8526, Japan (e-mail:ishikat{at}u-shizuoka-ken.ac.jp)






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