β_3-肾上腺素能受体对心力衰竭大鼠心室肌细胞内静息Ca^(2+)浓度的调控及其转导途径  

Regulation of resting intracellular Ca^(2+) concentration of ventricular myocytes by β_3-adrenoceptor and its signaling pathway in rats with experimental heart failure

作　　者：邓义军[1] 伍卫[2] 方昶[2] 黄至斌[2] 王景峰[2] 

机构地区：[1]盐城市第一人民医院ICU,江苏盐城224006 [2]中山大学附属第二医院心内科,广东广州510120

出　　处：《南方医科大学学报》2009年第8期1635-1637,1640,共4页Journal of Southern Medical University

基　　金：广东省医学科技基金(A2007184)

摘　　要：目的观察β3-肾上腺素能受体(β3-AR)对心力衰竭大鼠心室肌细胞内静息Ca2+浓度([Ca2+]i)的调控及其转导途径。方法通过结扎冠状动脉前降支制备大鼠实验性心力衰竭模型,经典酶分离法分离心肌细胞,Fluo-3/AM染色,激光共聚焦显微镜观察β3-AR兴奋剂BRL-37344以及合用PTX(Gi抑制剂)、L-NAME(NOS抑制剂)、Methylene blue(NO抑制剂)时对心室肌细胞内静息Ca2+浓度的影响及其转导途径。结果在心力衰竭和正常对照大鼠,β3-AR激动剂BRL37344(1μmol/L)分别使心室肌细胞内[Ca2+]i下调至用药前水平的59.4%、45.5%(P<0.05);在分别用L-NAME(10μmol/L)、Methylene blue(10μmol/L)、PTX(2μg/ml)阻断下,BRL37344(1μmol/L)使正常对照大鼠[Ca2+]i分别下降10.1%、16.9%、15.4%,而在心力衰竭大鼠[Ca2+]i分别下降16.9%、19.3%、11.7%。结论β3-AR激动剂可以使心室肌细胞内[Ca2+]i下调,心力衰竭心肌下调程度较轻,其作用是通过PTX-NOS-NO转导。Objective To observe the effect of β3-adrenoceptor (AR) in regulating resting intracellular Ca2+ concentration of the ventricular myocytes and investigate the signaling pathway in rats with experimental heart failure. Methods Rat models of experimental heart failure were established by ligation of the anterior descending artery, and the myocytes were isolated by enzymatic digestion. The resting intracellular Ca2+ concentration was determined using laser scanning confocal microscopy (LSCM) in the cells stimu...

关 键 词：Β3-肾上腺素能受体 心力衰竭 心室肌细胞 细胞内静息Ca2+浓度 

分 类 号：R541.6[医药卫生—心血管疾病]