长时间暴露于Ghrelin或GHRP-6对生长变异性GC细胞钾电流的影响

Belisario Domínguez Mancera, Eduardo Monjaraz Guzman, Jorge L V Flores-Hernández, Manuel Barrientos Morales, José M Martínez Hernandez, Antonio Hernández Beltran, Patricia Cervantes Acosta
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引用次数: 1

摘要

Ghrelin是一种生长激素(GH)分泌激素(GHS), GHRP-6是一种合成肽类似物;两者都通过GHS受体起作用。生长激素的分泌直接取决于细胞内Ca(2+)的浓度;这是由细胞内的储备和钙(2+)通过电压依赖性钙通道的进入决定的,这是由膜去极化激活的。膜电位主要由K(+)通道决定。在本研究中,我们研究了ghrelin (10 nM)和GHRP-6 (100 nM)作用96 h对大鼠GC细胞电压依赖性K(+)通道功能表达的影响。生理膜片钳全细胞记录仪记录K(+)电流。以Cd(2+) (1 mM)和河豚毒素(1 μ m)为记录液,根据其生物物理和药理学性质对三种电流进行表征。GC细胞的K(+)电流中含有对4-氨基吡啶敏感的瞬时组分(I a),约占总输出电流的40%;延迟整流器(ik),对四乙基铵敏感;第三种类型的K(+)电流被记录在电位大于负80mv时,允许K(+)进入,称为内向整流器(KIR)。长期使用ghrelin或GHRP-6治疗均未改变K(+)通道的功能表达,三种电流的振幅均无显著变化(P < 0.05);此外,它们的生物物理性质和动力学激活或失活没有改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Potassium Current Is Not Affected by Long-Term Exposure to Ghrelin or GHRP-6 in Somatotropes GC Cells.

Ghrelin is a growth hormone (GH) secretagogue (GHS) and GHRP-6 is a synthetic peptide analogue; both act through the GHS receptor. GH secretion depends directly on the intracellular concentration of Ca(2+); this is determined from the intracellular reserves and by the entrance of Ca(2+) through the voltage-dependent calcium channels, which are activated by the membrane depolarization. Membrane potential is mainly determined by K(+) channels. In the present work, we investigated the effect of ghrelin (10 nM) or GHRP-6 (100 nM) for 96 h on functional expression of voltage-dependent K(+) channels in rat somatotropes: GC cell line. Physiological patch-clamp whole-cell recording was used to register the K(+) currents. With Cd(2+) (1 mM) and tetrodotoxin (1  μ m) in the bath solution recording, three types of currents were characterized on the basis of their biophysical and pharmacological properties. GC cells showed a K(+) current with a transitory component (I A) sensitive to 4-aminopyridine, which represents ~40% of the total outgoing current; a sustained component named delayed rectifier (I K), sensitive to tetraethylammonium; and a third type of K(+) current was recorded at potentials more negative than -80 mV, permitting the entrance of K(+) named inward rectifier (KIR). Chronic treatment with ghrelin or GHRP-6 did not modify the functional expression of K(+) channels, without significant changes (P < 0.05) in the amplitudes of the three currents observed; in addition, there were no modifications in their biophysical properties and kinetic activation or inactivation.

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