目的：研究６β乙酰氧基去甲托烷（６βＡＮ）对支气管平滑肌的收缩作用．方法：不同ＭＲ拮抗剂对６βＡＮ作用的影响；ＨＰＬＣ法测定６βＡＮ对支气管平滑肌细胞内磷酸肌醇（ＩＰ）的影响；通过６βＡＮ对异丙肾上腺素（Ｉｓｏ）功能拮抗模型，观察６βＡＮ对Ｍ２Ｒ的作用．结果：（１）６βＡＮ对人及豚鼠气管的收缩强度大于ＡＣｈ，分别为６８和２４５倍；（２）阿托品（Ｍ１－Ｍ３）和ｐａｒａｆｌｕｏｒｏｈｅｘａｈｙｄｒｏｓｉｌａｄｉｆｅｎｉｄｏｌ（Ｍ３）抑制６βＡＮ的作用；（３）６βＡＮ引起平滑肌细胞内ＩＰ浓度升高；（４）６βＡＮ对Ｉｓｏ的功能性拮抗作用，在ｍｅｔｈｏｃｔｒａｍｉｎｅ（Ｍ２）０３μｍｏｌ·Ｌ－１时减弱或消失．结论：６βＡＮ通过激活Ｍ３Ｒ引起支气管平滑肌收缩；其对Ｉｓｏ的功能拮抗，部分是激活Ｍ２Ｒ所致． Objective: To study the contractile effect of 6β-acetoxy-nor-tropane (6β-AN) on bronchial smooth muscle. Methods: The effect of different M  R antagonists on the effect of 6βAN. The effect of 6βAN on phosphoinositide (IP) in bronchial smooth muscle cells was determined by HPLC. The function of isoproterenol (Iso) was antagonized by 6βAN Model to observe the effect of 6β-AN on M2  R. Results: (1) The contractile strength of 6βAN in trachea of ​​human and guinea pigs was higher than that of ACh by 68 and 245 times, respectively. (2) Atropine (M1-M3) and parafluorohexahydrosiladifenidol (M3) (3) 6β-AN induced a rise in IP concentration in smooth muscle cells; (4) The functional antagonism of 6β-AN to Iso attenuated or disappeared when methoctramine (M2) 03μmol·L-1 . Conclusion: 6β-AN caused by the activation of M3  R bronchial smooth muscle contraction; its functional antagonism of Iso, in part, is due to activation of M2  R.