缓激肽诱导牛气管平滑肌中环鸟苷酸积累的机制。

Mechanism of bradykinin-induced cyclic GMP accumulation in bovine tracheal smooth muscle.

作者信息

Sheng H, Ishii K, Förstermann U, Murad F

机构信息

Signal Transduction Group, Abbott Laboratories, Abbott Park, Illinois 60064, USA.

出版信息

Lung. 1995;173(6):373-83. doi: 10.1007/BF00172144.

DOI:10.1007/BF00172144

PMID:8531500

Abstract

Bradykinin (10(-8) - 10(-5) M) caused a concentration-dependent increase in cyclic GMP (cGMP) production in bovine tracheal smooth muscle in the absence of epithelium. The effect was calcium-dependent and was inhibited by pyrogallol (10 microM) and methylene blue (10 microM). The inhibition of pyrogallol was reversed by superoxide dismutase (100 U/ml). Nitric oxide (NO) synthase inhibitors, NG-methyl-L-arginine (10-100 microM) and NG-nitro-L-arginine (10-100 microM) reduced cGMP accumulation induced by bradykinin in a concentration-dependent fashion, and the inhibition was reversed by L-arginine. Immunohistochemistry with a specific antibody against neuronal NO synthase from rat cerebellum showed positive staining localized in some nerve fibers. Bradykinin-induced cGMP accumulation appears to be related to the release of NO, part of which is probably synthesized in nonadrenergic noncholinergic nerve in bovine trachea.

摘要

在无上皮的牛气管平滑肌中，缓激肽（10⁻⁸ - 10⁻⁵ M）可引起环磷酸鸟苷（cGMP）生成呈浓度依赖性增加。该效应依赖于钙，并被焦性没食子酸（10 μM）和亚甲蓝（10 μM）抑制。超氧化物歧化酶（100 U/ml）可逆转焦性没食子酸的抑制作用。一氧化氮（NO）合酶抑制剂N⁻甲基⁻L⁻精氨酸（10 - 100 μM）和N⁻硝基⁻L⁻精氨酸（10 - 100 μM）以浓度依赖性方式降低缓激肽诱导的cGMP积累，且L⁻精氨酸可逆转该抑制作用。用来自大鼠小脑的抗神经元型NO合酶特异性抗体进行免疫组织化学显示，阳性染色定位于一些神经纤维中。缓激肽诱导的cGMP积累似乎与NO的释放有关，其中一部分可能在牛气管的非肾上腺素能非胆碱能神经中合成。