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目的 :探讨信使分子IP3 在M3 R介导逼尿肌细胞收缩中的作用。方法 :MR非选择性的激动剂 (carba chol)、拮抗剂 (atropine)及M2 R拮抗剂 (methoctramine)、M3 R拮抗剂 (4-DAMP)刺激原代培养人逼尿肌细胞 ,通过 [3 H]掺入法 ,检测磷脂酰肌醇 (PI)的代谢产物 [3 H]-IP含量。结果 :[3 H]-IP的含量随carbachol刺激浓度的增加而增加 ;atropine和 4 -DAMP能显著抑制carbachol诱导的代谢反应 (P <0 .0 1) ,而methoc tramine不能显著抑制carbachol的作用 ;atropine与 4 -DAMP的作用相比无显著性差异 (P >0 .0 5 )。结论 :M3 R与PI分解产生的第二信使分子IP3 密切相关。
Objective: To investigate the role of messenger molecule IP3 in M3 R-mediated contraction of detrusor myocytes. Methods: MR dexamethasone was used to stimulate human primary detrusor myocytes cultured with carotenoid, atropine, M2R antagonist and M3 R antagonist (4-DAMP) H] incorporation method was used to detect the metabolite [3 H] -IP content of phosphatidylinositol (PI). Results: The content of [3 H] -IP increased with the increase of carbachol concentration; atropine and 4-DAMP significantly inhibited the carbachol-induced metabolic reaction (P <0.01), but methoc tramine did not significantly inhibit the effect of carbachol There was no significant difference between atropine and 4-DAMP (P> 0.05). Conclusion: M3 R is closely related to IP3, a second messenger molecule produced by PI.