异搏定引致人类β肾上腺素能受体的耦合增强效应

Verapamil-Induced Enhancement of Coupling in Human Beta—adrenergic Receptors

本实验从同时暴露于异搏定中的正常人白细胞β肾上腺素能受体所产生的异丙肾竟争曲线来分析可见,异搏定可引起KL/KH比值升高38%(P<0.035)。而受体数目、高亲和力状态受体所占比率,以及拮抗亲和力状态受体所占比率等均无相应的改变。因而,在异搏定治疗过程中,所观察到的异丙肾刺激所致的腺甙酸环化酶活性增高的现象,至少部分地是由于异搏定增强耦合效应的一种直接性影响。

Isoproterenol competition curves were created from normal neutrophil beta-adrenergic receptors coexposed to verapamil. In comparison with the controls there was a 38% verapamil-induced rise in K^L/K^H (P<0.035). There were no corresponding changes in the number of receptors, the proportion of receptors in the high affinity state, and in antagonist affinity. Thus the increased isoproterenol-stimulated adenylate cyclase activity observed during verapamil therapy was not solely the consequence of homologous supersensitivity, but was due at least in part to a direct of verapamil to enhance coupling.