Department of Physiology, Medical College of Nanchang University, Nanchang, Jiangxi 330006, PR China.
Neurochem Int. 2013 Sep;63(3):230-7. doi: 10.1016/j.neuint.2013.06.003. Epub 2013 Jun 14.
Myocardial ischemic injury activates cardiac sympathetic afferent fibers and elicits a sympathoexcitatory reflex by exciting sympathetic efferent action, with resultant augmentation of myocardial oxygen consumption, leading to a vicious cycle of exaggerating myocardial ischemia. P2X7 receptor participates in the neuronal functions and the neurological disorders. This study examined the role of P2X7 receptor of superior cervical ganglia (SCG) in sympathoexcitatory reflex. Our results showed that the expression of P2X7 receptor at both mRNA and protein in SCG was increased after myocardial ischemic injury. P2X7 receptor agonists at the same concentration activated much larger amplitudes of the currents in the SCG neurons of myocardial ischemic rats than those in control rats. P2X7 receptor antagonist (brilliant blue G, BBG) significantly inhibited P2X7 receptor agonist-activated currents in the SCG neurons. Excessive phosphorylation of MAPK ERK1/2 upon the activation of P2X7 receptor might be a mechanism mediating the signal transduction after myocardial ischemic injury. Therefore, the sensitized P2X7 receptor in SCG was involved in the nociceptive transmission of sympathoexcitatory reflex induced by myocardial ischemic injury.
心肌缺血损伤通过兴奋交感传出活动激活心脏交感传入纤维，引发交感兴奋反射，导致心肌耗氧量增加，从而形成加剧心肌缺血的恶性循环。P2X7 受体参与神经元功能和神经紊乱。本研究探讨了颈上神经节（SCG）中 P2X7 受体在交感兴奋反射中的作用。我们的结果表明，心肌缺血损伤后，SCG 中 P2X7 受体的 mRNA 和蛋白表达均增加。相同浓度的 P2X7 受体激动剂在心肌缺血大鼠的 SCG 神经元中激活的电流幅度远大于对照组大鼠。P2X7 受体拮抗剂（亮蓝 G，BBG）显著抑制了 SCG 神经元中 P2X7 受体激动剂激活的电流。P2X7 受体激活后 MAPK ERK1/2 的过度磷酸化可能是介导心肌缺血损伤后信号转导的机制。因此，SCG 中致敏的 P2X7 受体参与了心肌缺血损伤引起的交感兴奋反射的伤害性传递。
