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Involvement of stretch-activated cation channels in hypotonically induced insulin secretion in rat pancreatic [beta]-cells
In isolated rat pancreatic ...-cells, hypotonic stimulation elicited an increase in cytosolic Ca2+ concentration (...) at 2.8 mM glucose. The hypotonically induced ... elevation was significantly suppressed by nicardipine, a voltage-dependent Ca2+ channel blocker, and by Gd... amiloride, 2-aminoetho...
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Published in: | American Journal of Physiology: Cell Physiology 2006-12, Vol.291 (6), p.C1405 |
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container_title | American Journal of Physiology: Cell Physiology |
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creator | Takii, Miki Ishikawa, Tomohisa Tsuda, Hidetaka Kanatani, Kazumitsu |
description | In isolated rat pancreatic ...-cells, hypotonic stimulation elicited an increase in cytosolic Ca2+ concentration (...) at 2.8 mM glucose. The hypotonically induced ... elevation was significantly suppressed by nicardipine, a voltage-dependent Ca2+ channel blocker, and by Gd... amiloride, 2-aminoethoxydiphenylborate, and ruthenium red, all cation channel blockers. In contrast, the ... elevation was not inhibited by suramin, a P... purinoceptor antagonist. Whole cell patch-clamp analyses showed that hypotonic stimulation induced membrane depolarization of ...-cells and produced outwardly rectifying cation currents; Gd... inhibited both responses. Hypotonic stimulation also increased insulin secretion from isolated rat islets, and Gd... significantly suppressed this secretion. Together, these results suggest that osmotic cell swelling activates cation channels in rat pancreatic ...-cells, thereby causing membrane depolarization and subsequent activation of voltage-dependent Ca2+ channels and thus elevating insulin secretion. (ProQuest Information and Learning: ... denotes formulae omitted.) |
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The hypotonically induced ... elevation was significantly suppressed by nicardipine, a voltage-dependent Ca2+ channel blocker, and by Gd... amiloride, 2-aminoethoxydiphenylborate, and ruthenium red, all cation channel blockers. In contrast, the ... elevation was not inhibited by suramin, a P... purinoceptor antagonist. Whole cell patch-clamp analyses showed that hypotonic stimulation induced membrane depolarization of ...-cells and produced outwardly rectifying cation currents; Gd... inhibited both responses. Hypotonic stimulation also increased insulin secretion from isolated rat islets, and Gd... significantly suppressed this secretion. Together, these results suggest that osmotic cell swelling activates cation channels in rat pancreatic ...-cells, thereby causing membrane depolarization and subsequent activation of voltage-dependent Ca2+ channels and thus elevating insulin secretion. 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The hypotonically induced ... elevation was significantly suppressed by nicardipine, a voltage-dependent Ca2+ channel blocker, and by Gd... amiloride, 2-aminoethoxydiphenylborate, and ruthenium red, all cation channel blockers. In contrast, the ... elevation was not inhibited by suramin, a P... purinoceptor antagonist. Whole cell patch-clamp analyses showed that hypotonic stimulation induced membrane depolarization of ...-cells and produced outwardly rectifying cation currents; Gd... inhibited both responses. Hypotonic stimulation also increased insulin secretion from isolated rat islets, and Gd... significantly suppressed this secretion. Together, these results suggest that osmotic cell swelling activates cation channels in rat pancreatic ...-cells, thereby causing membrane depolarization and subsequent activation of voltage-dependent Ca2+ channels and thus elevating insulin secretion. 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The hypotonically induced ... elevation was significantly suppressed by nicardipine, a voltage-dependent Ca2+ channel blocker, and by Gd... amiloride, 2-aminoethoxydiphenylborate, and ruthenium red, all cation channel blockers. In contrast, the ... elevation was not inhibited by suramin, a P... purinoceptor antagonist. Whole cell patch-clamp analyses showed that hypotonic stimulation induced membrane depolarization of ...-cells and produced outwardly rectifying cation currents; Gd... inhibited both responses. Hypotonic stimulation also increased insulin secretion from isolated rat islets, and Gd... significantly suppressed this secretion. Together, these results suggest that osmotic cell swelling activates cation channels in rat pancreatic ...-cells, thereby causing membrane depolarization and subsequent activation of voltage-dependent Ca2+ channels and thus elevating insulin secretion. 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subjects | Calcium Cellular biology Glucose Insulin Ions |
title | Involvement of stretch-activated cation channels in hypotonically induced insulin secretion in rat pancreatic [beta]-cells |
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