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Properties of calcium channels coupled to endogenous glutamate release from the vascularly perfused rat stomach in vitro.

机译:钙通道的特性与内源性谷氨酸在体外从血管灌注的大鼠胃中释放有关。

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摘要

We have demonstrated that both high-K+ and electrical stimulation of the vagus nerves release endogenous glutamate from the vascularly-perfused rat stomach in a calcium-dependent manner. In the present study, we examined properties of calcium channel subtypes mediating endogenous glutamate release from the stomach. Application of 50 mM KCl elicited a release of glutamate, and this release was abolished in calcium-free medium. The release of glutamate was significantly inhibited by both omega-agatoxin IVA, a P/Q-type calcium channel antagonist, and isradipine, an L type calcium channel antagonist. Omega-conotoxin GVIA, an N type calcium channel antagonist and flunarizine, a nonselective T-type calcium channel antagonist were without effect. In contrast to this case of glutamate, omega-conotoxin GVIA induced a marked inhibition in the release of gastric noradrenaline. The combined treatment with omega-agatoxin IVA plus isradipine produced a marked synergistic inhibition of the glutamate release. This inhibition was, however, much less than that by cadmium. The present results suggest that P/Q and L type calcium channels coexist to regulate the release of gastric glutamate. Furthermore, it is possible that unidentified calcium channels other than P/Q and L type channels are also involved in the release of glutamate in the stomach.
机译:我们已经证明迷走神经的高K +和电刺激都以钙依赖的方式从血管灌注的大鼠胃中释放出内源性谷氨酸。在本研究中,我们检查了介导内源性谷氨酸从胃中释放的钙通道亚型的特性。 50 mM KCl的施加引起谷氨酸释放,并且该释放在无钙培养基中被消除。谷氨酸的释放被P / Q型钙通道拮抗剂ω-agagaxin毒素IVA和L型钙通道拮抗剂伊拉地平均显着抑制。 N型钙通道拮抗剂Omega-conotoxin GVIA和非选择性T型钙通道拮抗剂氟那利嗪无效。与这种谷氨酸相反,ω-芋螺毒素GVIA在胃去甲肾上腺素的释放中具有明显的抑制作用。欧米加-琼脂毒素IVA加伊拉地平的联合治疗对谷氨酸的释放产生了明显的协同抑制作用。但是,这种抑制作用远小于镉。目前的结果表明,P / Q和L型钙通道共存以调节胃谷氨酸的释放。此外,除P / Q和L型通道外,其他未知的钙通道也可能与谷氨酸在胃中的释放有关。

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