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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
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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.
出处 《四川医学》 CAS 2012年第3期383-385,共3页 Sichuan Medical Journal
关键词 肾上腺能β3受体 逼尿肌细胞 钙调蛋白 β3-adrenoceptors detrusor cell calcium calmodulin
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