Restraint stress induces connexin-43 translocation in rat heart

静止（IMO）会给动物和人类带来情绪压力。最近有报道称，大鼠的IMO诱导连接蛋白43（Cx43）易位至间隙连接（GJs），并通过GJ抑制减弱心律失常。很少有报道显示肾上腺素受体在心肌细胞中对Cx43上调的贡献，但肾上腺素受体和缺血在心肌组织中Cx43易位的参与仍然是未知的。雄性Sprague-Dawley大鼠进行IMO， western blotting检测Cx43在脑室的分布。IMO诱导Cx43向富含gj的膜部分易位，在60min时达到峰值。α-肾上腺素受体预处理可抑制imo诱导的Cx43易位。β受体阻滞剂可抑制IMO引起的室性早搏。Cx43向gj富集部分的易位是通过α-肾上腺素受体途径发生的，与缺血无关。β-肾上腺素受体途径参与了IMO中室性早搏的诱导

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