肾上腺素β_3受体调节大鼠逼尿肌舒张的机制  

The mechanism of beta3-adrenoceptors mediated rat ditrusor relaxation

作　　者：曹文锋[1] 王亮[1] 王庆堂[1] 杨航[1] 陈卫国[1] 李沙丹[1] 

机构地区：[1]成都军区总医院泌尿外科,四川成都610083

出　　处：《四川医学》2012年第3期383-385,共3页Sichuan Medical Journal

摘　　要：目的探讨肾上腺能β3受体(β3-AR)调节逼尿肌舒张的机制。方法应用激光共聚焦显微镜观察不同浓度β3-AR激动剂BRL37344A对氯化钾和咖啡因诱发的大鼠逼尿肌细胞钙荧光强度的变化,流式细胞仪测定β3-AR激活后细胞内CaM活性变化。结果较高浓度(1×10-6mmol/L及1×10-4mmol/L)的BRL37344A分别使氯化钾诱发的细胞内钙荧光强度的峰值下降了18.2%和28.3%,而低浓度BRL37344A对氯化钾诱发的细胞钙离子跨膜内流无显著影响;不同浓度的BRL37344对咖啡因诱发的细胞肌浆网内储存钙的释放均无明显影响(P>0.05)。β3-AR激活后细胞内活性CaM含量明显增加。结论 BRL37344A抑制电压门控钙通道的开放,减少钙离子跨膜内流。Ca2+-CaM信号传导途径参与了β3-AR介导逼尿肌细胞舒张调节过程。Objective To explore the mechanism of β3-adrenoceptors on detrusor relaxation.Methods The effects of BRL37344A in different concentration on the change of intracellular Ca2＋ concentration induced by KCl and caffeine were detected with confocal laser scanning microscopy by using Ca2＋ sensitive dye fluo-3AM as calcium fluorescent.The CaM fluorescence density determined.Results Higher concentration BRL37344A（10-6 mmol·L-1 and 10-4 mmol·L） could inhibit Ca2＋ transsarcolemmal influx induced by KCl（peak Ca2＋ fluorescent intensity decreased 18.2% and 28.3%）,but low concentration BRL37344A did not（P0.05）.BRL37344A did not altered the amount of Ca2＋ releaes from intracellular stores responsed to caffeine.Afterβ3-AR stimulated by BRL37344A,intracellular CaM activity relatively were increased.Conclusion The negative inotropic effects of BRL37344A may be mediated by decrease Ca2＋ transsarcolemmal influx through voltage-gated calcium channel.β3-AR mediated detrusor relaxation was completed by the Ca2＋-CaM signal pathway.

关 键 词：肾上腺能β3受体 逼尿肌细胞 钙 钙调蛋白 

分 类 号：R-332[医药卫生]