Electrophysiological studies of upregulated P2X7 receptors in rat superior cervical ganglia after myocardial ischemic injury

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. P2X(7) receptor participates in the neuronal functions and the neurological disorders. This study examined the role of P2X(7) receptor of superior cervical ganglia (SCG) in sympathoexcitatory reflex. Our results showed that the expression of P2X(7) receptor at both mRNA and protein in SCG was increased after myocardial ischemic injury. P2X(7) 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. P2X(7) receptor antagonist (brilliant blue G, BBG) significantly inhibited P2X(7) receptor agonist-activated currents in the SCG neurons. Excessive phosphorylation of MAPK ERK1/2 upon the activation of P2X(7) receptor might be a mechanism mediating the signal transduction after myocardial ischemic injury. Therefore, the sensitized P2X(7) receptor in SCG was involved in the nociceptive transmission of sympathoexcitatory reflex induced by myocardial ischemic injury. (C) 2013 Elsevier Ltd. All rights reserved.