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前肾上腺髓质素氨基末端20肽通过大鼠嗜铬细胞瘤衍生的PC 12细胞中对百日咳毒素敏感的G蛋白抑制电压门控Ca2+通道电流。

Proadrenomedullin NH2-terminal 20 peptide inhibits the voltage-gated Ca2+ channel current through a pertussis toxin-sensitive G protein in rat pheochromocytoma-derived PC 12 cells.

作者信息

Takano K, Yamashita N, Fujita T

机构信息

Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.

出版信息

J Clin Invest. 1996 Jul 1;98(1):14-7. doi: 10.1172/JCI118758.

DOI:10.1172/JCI118758
PMID:8690785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC507394/
Abstract

The effect of proadrenomedullin NH2-terminal 20 peptide (PAMP) on the voltage-gated Ca2+ channel current was investigated using the perforated whole-cell clamp technique on NGF-treated PC12 cells. PAMP inhibited the Ba2+ current through N-type Ca2+ channels in a concentration dependent manner. Injection of GDPbetaS into the cell abolished the inhibition while injection of GTPgammaS into the cell made the inhibition irreversible, indicating that the PAMP-induced inhibition of the voltage-gated Ca2+ channel was mediated by a G protein. The inhibition was abolished by pretreating the cells with pertussis toxin, indicating that a pertussis toxin-sensitive G protein was involved in the signal transduction mechanism of PAMP. The present study revealed that the inhibition of catecholamine secretion from sympathetic nerve endings by PAMP could be explained by the inhibition of N-type Ca2+ channels, which was mediated by pertussis toxin-sensitive G protein.

摘要

采用穿孔全细胞膜片钳技术，在经神经生长因子（NGF）处理的PC12细胞上研究了肾上腺髓质素NH2末端20肽（PAMP）对电压门控性Ca2+通道电流的影响。PAMP以浓度依赖性方式抑制通过N型Ca2+通道的Ba2+电流。向细胞内注射GDPβS可消除这种抑制作用，而向细胞内注射GTPγS则使这种抑制作用不可逆，这表明PAMP诱导的电压门控性Ca2+通道抑制是由G蛋白介导的。用百日咳毒素预处理细胞可消除这种抑制作用，表明百日咳毒素敏感的G蛋白参与了PAMP的信号转导机制。本研究表明，PAMP对交感神经末梢儿茶酚胺分泌的抑制作用可通过对N型Ca2+通道的抑制来解释，而这种抑制是由百日咳毒素敏感的G蛋白介导的。

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本文引用的文献

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