title: P2X2/3 receptor activity of rat nodose ganglion neurons contributing to myocardial ischemic nociceptive signaling.
abstract: Myocardial ischemia causes the production of a variety of chemical substances, which act on the cardiac afferent nerve to cause pain. Myocardial damage can affect cardiac vagal afferent activity. Survivors of myocardial infarction are often left with impaired activity of cardiac vagal sensory fibres. The nodose ganglia (NG) are lower ganglia of cardiac vagus nerve, which are chiefly visceral afferent in the sensation of heart. ATP as a possible damage signal may activate nociceptive sensory neurons. Activation of P2X(3), P2X(2/3) receptors by endogenous ATP contributes to the development of hyperalgesia. The present results have shown that the sensitivity of P2X(2/3) receptor in nodose ganglion neurons was increased after myocardial ischemic injury under electrophysiological observation. The inhibitive role of P2X(2/3) antagonist A-317491 on ATP-activated currents in myocardial ischemic rats was significantly increased, compared with that in control group at the same concentration of A-317491. The staining of P2X(2) and P2X(3) receptors in myocardial ischemic injury group appeared to be more intense than those in naive rats and myocardial ischemic rats treated with A-317491 with immunofluorescence double labeling methods. Therefore, the activity of P2X(2/3) receptors in NG neurons was involved in the transmission of myocardial ischemic nociceptive signal.
authors.affiliation: Department of Physiology, Basic Medical College of Nanchang University, Nanchang 330006, PR China.
authors.forename: Fang
authors.initials: F
authors.lastname: Wan
authors.forename: Guilin
authors.initials: G
authors.lastname: Li
authors.forename: Shuangmei
authors.initials: S
authors.lastname: Liu
authors.forename: Gaochun
authors.initials: G
authors.lastname: Zhu
authors.forename: Changshui
authors.initials: C
authors.lastname: Xu
authors.forename: Jiari
authors.initials: J
authors.lastname: Lin
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.forename: Shangdong
authors.initials: S
authors.lastname: Liang
mesh_terms: D000787:Angina Pectoris / Q000209:etiology / Q000378:metabolism*; D000818:Animals; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D009434:Neural Pathways / Q000502:physiology; D009619:Nociceptors / Q000502:physiology*; D009620:Nodose Ganglion / Q000502:physiology*; D010636:Phenols / Q000494:pharmacology; D011083:Polycyclic Compounds / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D058469:Receptors, Purinergic P2X / Q000378:metabolism* / Q000502:physiology; D058477:Receptors, Purinergic P2X3 / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
chemical_list: C470346:A-317491; D010636:Phenols; D011083:Polycyclic Compounds; D058469:Receptors, Purinergic P2X; D058477:Receptors, Purinergic P2X3