毒蕈碱的M (3) receptor-dependent调节气道平滑肌收缩表型。

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Gosens R, Bromhaar MM,坦克,Schaafsma D, Zaagsma J,内尔SA穆尔H

毒蕈碱的M (3) receptor-dependent调节气道平滑肌收缩表型。

Br J杂志。2004年3月,141 (6):943 - 50。doi: 10.1038 / sj.bjp.0705709。Epub 2004 3月1。

PubMed ID

14993104 (在PubMed

]

文摘

1。气道平滑肌细胞(ASM)已知开关从一个收缩的增殖和合成表型文化在血清和生长因子。表型转换收缩受体激动剂,但是,不好描述,尽管可能ASM表型之间的关系,在哮喘气道重塑。2。探讨毒蕈碱的受体刺激ASM表型的影响,我们使用organ-cultured牛气管平滑肌(BTSM)条收缩反应,收缩蛋白表达和增殖是测量与醋甲胆碱预处理后。3所示。长期醋甲胆碱预处理(8天)最大收缩和对乙酰甲胆碱的敏感性以及减少组胺和氯化钾。这种减少摄入量有关(压电陶瓷(50)= 5.2 + / - -0.1)。预处理浓度最高的醋甲胆碱应用(100 microm)会抑制最大histamine-induced收缩控制8 + / - -1%。此外,收缩蛋白表达(肌球蛋白、肌动蛋白)表达下调是双重的。 No concomitant increase in proliferative capacity was observed. 4. The M(3)/M(2) muscarinic receptor antagonist DAU 5884 (0.1 microm) completely inhibited the observed decrease in contractility. In contrast, the M(2)/M(3) muscarinic receptor antagonist gallamine (10 microm) was ineffective, demonstrating that M(2) receptors were not involved. 5. Pretreatment (8 days) with 60 mm KCl could mimick the strong decreases in contractility. This was completely prevented by pretreatment with verapamil (1 microm). 6. Regulation of contractility was not affected by protein kinase C inhibition, whereas inhibitors of phosphatidyl inositol 3-kinase and p42/p44 mitogen activated protein kinase were partially effective. 7. These results show that long-term methacholine pretreatment (8 days) induces an M(3) receptor-dependent decrease in BTSM contractility without increased proliferative capacity.

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药物

醋甲胆碱

药物靶点

药物	目标	类	生物	药理作用	行动
醋甲胆碱	毒蕈碱的乙酰胆碱受体M3	蛋白质	人类	是的	受体激动剂	细节