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目的 探讨β3 AR介导大鼠逼尿肌细胞舒张的信号转导途径。方法 采用放射免疫法测cAMP浓度 ,细胞功能实验观察cAMP特异性拮抗剂SQ 2 2 ,5 36和PKA特异性拮抗剂H 89对β AR激动剂异丙肾上腺素 (ISO)及β3 AR激动剂BRL37344A调节逼尿肌细胞舒张作用的影响。结果 ISO能增加细胞内cAMP含量 ,SQ 2 2 ,5 36和H 89均可部分抑制ISO对逼尿肌细胞的松弛作用 ,而BRL37344A对逼尿肌细胞内cAMP水平无明显影响 ,SQ 2 2 ,5 36和H 89不能抑制BRL37344A介导的逼尿肌细胞松弛作用。结论 β AR通过依赖和不依赖cAMP PKA的多种信号转导途径调节逼尿肌舒张 ,而cAMP PKA途径未参与β3 AR调节逼尿肌舒张的作用
Aim To investigate the signal transduction pathways of β3 AR-mediated relaxation in detrusor cells of rats. Methods The concentration of cAMP was measured by radioimmunoassay. The effect of cAMP specific antagonist SQ 2 2, 5 36 and PKA specific antagonist H 89 on isoproterenol (ISO) and β 3 AR agonist BRL37344A Regulate the effect of detrusor cell relaxation. Results ISO increased the intracellular cAMP level. SQ2 2, 5 36 and H 89 both partially inhibited the relaxation of ISO to detrusor cells. However, BRL37344A had no significant effect on cAMP level in detrusor cells. SQ 2 2, 5 36 and H 89 failed to inhibit BRL37344A mediated detrusor relaxation. Conclusion β AR modulates detrusor relaxation by a variety of signal transduction pathways dependent and independent of cAMP PKA, whereas cAMP PKA pathway is not involved in the regulation of detrusor relaxation by β 3 AR