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首页> 外文期刊>Bioscience Reports >Alpha2-adrenoreceptor stimulation does not inhibit L-type calcium channels in mouse pancreatic β-cells
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Alpha2-adrenoreceptor stimulation does not inhibit L-type calcium channels in mouse pancreatic β-cells

机译:α2肾上腺素能受体刺激不会抑制小鼠胰腺β细胞的L型钙通道

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The effects of α2-adrenergic stimulation on the Ca2+-current in mouse pancreatic β-cells were investigated using the patch-clamp technique. When using the conventional whole-cell recording configuration (dialysis of cell interior with pipette solution), addition of adrenaline (1 μM) or the α2-adrenergic agonist clonidine (5 μM) failed to reduce the Ca2+-current, irrespective of whether intracellular GTP (or GTPγ S) was present or not and at both physiological (1.3 mM) and elevated (10.2 mM) Ca2+-concentrations. In fact, in the absence of added guanine nucleotides, the agonists tended to increase the Ca2+-current amplitude in the presence of the higher Ca2+-concentration. Ca2+-channel activation measured at 1.3 mM Ca2+ was not affected by clonidine. Half-maximal activation was observed at ≈?20 mV. In addition, when Ca2+-currents were recorded from intact β-cells, using the perforated patch whole-cell configuration, clonidine (1 μM) also failed to detectably affect the Ca2+-current. It is therefore suggested that the inhibition of β-cell electrical activity and insulin-secretion produced by α2-adrenoreceptor stimulation does not result from suppression of the L-type Ca2+-current.
机译:使用膜片钳技术研究了α2-肾上腺素能刺激对小鼠胰腺β细胞Ca2 +电流的影响。当使用常规的全细胞记录配置(用移液器透析细胞内部)时,无论细胞内是否存在GTP,添加肾上腺素(1μM)或α2-肾上腺素能激动剂可乐定(5μM)都无法降低Ca2 +电流。 (或GTPγS)的存在与否以及生理(1.3 mM)和升高(10.2 mM)的Ca2 +浓度。实际上,在不存在鸟嘌呤核苷酸的情况下,在较高的Ca2 +浓度下,激动剂倾向于增加Ca2 +-电流幅度。在1.3 mM Ca2 +下测得的Ca2 +通道激活不受可乐定影响。在≈?20 mV处观察到半最大激活。此外,当从完整的β细胞中记录Ca2 +电流时,使用穿孔的贴片全细胞配置,可乐定(1μM)也未能可检测地影响Ca2 +电流。因此表明,α2肾上腺素受体刺激产生的β细胞电活性抑制和胰岛素分泌不是由抑制L型Ca 2+电流引起的。

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