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8-溴环鸟苷酸通过蛋白激酶A介导气管平滑肌舒张。

8Br-cGMP mediates relaxation of tracheal smooth muscle through PKA.

作者信息

Algara-Suárez Paola, Espinosa-Tanguma Ricardo

机构信息

Departamento de Fisiología y Farmacología, Facultad de Medicina, Universidad Autónoma de San Luis Potosi, S.L.P. 78210, San Luis Potosí, Mexico.

出版信息

Biochem Biophys Res Commun. 2004 Feb 6;314(2):597-601. doi: 10.1016/j.bbrc.2003.12.136.

Abstract

In this study, guinea pig tracheal smooth muscle pre-contracted with histamine was relaxed by the addition of 100microM 8Br-cGMP, a non-hydrolyzable and cell-permeable analog for cGMP. This effect was not sensitive to cGMP-dependent protein kinase (PKG) inhibitors, whereas it was partially blocked by cAMP-dependent protein kinase (PKA) inhibitors. The relaxation observed was also reverted up to 50+/-8.5% by iberiotoxin, a selective inhibitor of large conductance, calcium-activated potassium channels (BK(Ca)). Our results indicate that there exists a crosstalk mechanism between cAMP and cGMP signaling pathways which lead to relaxation of guinea pig tracheal smooth muscle and also that BK(Ca) channels are involved to a certain extent in this phenomenon.

摘要

在本研究中,用组胺预收缩的豚鼠气管平滑肌通过添加100微摩尔的8-溴环鸟苷酸(8Br-cGMP,一种不可水解且可透过细胞的环鸟苷酸类似物)而松弛。这种效应对环鸟苷酸依赖性蛋白激酶(PKG)抑制剂不敏感,而部分被环磷酸腺苷依赖性蛋白激酶(PKA)抑制剂阻断。所观察到的松弛也被iberiotoxin(一种大电导钙激活钾通道(BK(Ca))的选择性抑制剂)逆转高达50±8.5%。我们的结果表明,环磷酸腺苷(cAMP)和环鸟苷酸(cGMP)信号通路之间存在一种相互作用机制,该机制导致豚鼠气管平滑肌松弛,并且BK(Ca)通道在这一现象中也有一定程度的参与。

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