Restraint stress induces connexin-43 translocation in rat heart

固定（IMO）赋予动物和人类的情绪压力。最近有研究表明，IMO可诱导大鼠缝隙连接蛋白43（Cx43）易位到缝隙连接（GJ），并通过抑制GJ来减弱大鼠的肿瘤发生。很少有报道表明，在心肌细胞中的Cx43上调的肾上腺素受体的贡献，但在IMO Cx43易位的肾上腺素受体和缺血的参与仍然是难以捉摸的。雄性Sprague-Dawley大鼠进行IMO，并通过蛋白质印迹法检测Cx43的心室分布。IMO诱导Cx43向富含GJ的膜组分移位，峰值在60 min。用α-肾上腺素能受体预处理可抑制IMO诱导的Cx43易位。β受体阻滞剂可抑制IMO诱发的室性早搏（PVC）。Cx43通过α-肾上腺素受体途径转运至GJ富集组分，与缺血无关。β-肾上腺素受体通路参与了IMO中PVC的诱导

Immobilization(IMO) confers emotional stress in animals and humans. It was recently reported that IMO in rats induced translocation of connexin-43(Cx43) to gap junctions(GJs) and attenuated arrhythmogenesis with GJ inhibition. Few reports show the contribution of adrenoceptors to Cx43 upregulation in cardiomyocytes, but the involvement of adrenoceptors and ischemia in Cx43 translocation in IMO remains elusive. Male Sprague-Dawley rats underwent IMO and the ventricular distribution of Cx43 was examined by western blotting. IMO induced translocation of Cx43 to the GJ-enriched membrane fraction, with a peak at 60min. The IMO-induced Cx43 translocation was inhibited by pretreatment with theα-adrenoceptor. Theβ-blockers inhibited the premature ventricular contractions(PVCs) induced by IMO. Translocation of Cx43 to the GJ-enriched fraction occurs via theα-adrenoceptor pathway, independently of ischemia. Theβ-adrenoceptor pathway contributes to the inducing of PVCs in IMO