| Autor: |
Takii, Miki, Ishikawa, Tomohisa, Tsuda, Hidetaka, Kanatani, Kazumitsu, Sunouchi, Takaaki, Kaneko, Yukiko, Nakayama, Koichi |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Cell Physiology; Dec2006, Vol. 291 Issue 6, pC1405-C1411, 7p, 19 Graphs |
| Abstrakt: |
In isolated rat pancreatic β-cells, hypotonic stimulation elicited an increase in cytosolic Ca2+ concentration ([Ca2+J~) at 2.8 mM glucose. The hypotonically induced [Ca2+]i 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+]~ elevation was not inhibited by suramin, a P2 purinoceptor antagonist. Whole cell patch-clamp analyses showed that hypotonic stimulation induced membrane depolarization of β-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 β-cells, thereby causing membrane depolarization and subsequent activation of voltage-dependent Ca2+ channels and thus elevating insulin secretion. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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