title: Sensory-sympathetic coupling in superior cervical ganglia after myocardial ischemic injury facilitates sympathoexcitatory action via P2X7 receptor.
abstract: P2X receptors participate in cardiovascular regulation and disease. After myocardial ischemic injury, sensory-sympathetic coupling between rat cervical DRG nerves and superior cervical ganglia (SCG) facilitated sympathoexcitatory action via P2X7 receptor. The results showed that after myocardial ischemic injury, the systolic blood pressure, heart rate, serum cardiac enzymes, IL-6, and TNF-α were increased, while the levels of P2X7 mRNA and protein in SCG were also upregulated. However, these alterations diminished after treatment of myocardial ischemic (MI) rats with the P2X7 antagonist oxATP. After siRNA P2X7 in MI rats, the systolic blood pressure, heart rate, serum cardiac enzymes, the expression levels of the satellite glial cell (SGC) or P2X7 were significantly lower than those in MI group. The phosphorylation of ERK 1/2 in SCG participated in the molecular mechanism of the sympathoexcitatory action induced by the myocardial ischemic injury. Retrograde tracing test revealed the sprouting of CGRP or SP sensory nerves (the markers of sensory afferent fibers) from DRG to SCG neurons. The upregulated P2X7 receptor promoted the activation of SGCs in SCG, resulting in the formation of sensory-sympathetic coupling which facilitated the sympathoexcitatory action. P2X7 antagonist oxATP could inhibit the activation of SGCs and interrupt the formation of sensory-sympathetic coupling in SCG after the myocardial ischemic injury. Our findings may benefit the treatment of coronary heart disease and other cardiovascular diseases.
authors.affiliation: Department of Physiology, Medical College of Nanchang University, Nanchang, Jiangxi, 330006, People's Republic of China.
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.forename: Guilin
authors.initials: G
authors.lastname: Li
authors.forename: Haiying
authors.initials: H
authors.lastname: Peng
authors.forename: Guihua
authors.initials: G
authors.lastname: Tu
authors.forename: Fanjun
authors.initials: F
authors.lastname: Kong
authors.forename: Shuangmei
authors.initials: S
authors.lastname: Liu
authors.forename: Yun
authors.initials: Y
authors.lastname: Gao
authors.forename: Hong
authors.initials: H
authors.lastname: Xu
authors.forename: Shuyi
authors.initials: S
authors.lastname: Qiu
authors.forename: Bo
authors.initials: B
authors.lastname: Fan
authors.forename: Qicheng
authors.initials: Q
authors.lastname: Zhu
authors.forename: Shicheng
authors.initials: S
authors.lastname: Yu
authors.forename: Chaoran
authors.initials: C
authors.lastname: Zheng
authors.forename: Bing
authors.initials: B
authors.lastname: Wu
authors.forename: Lichao
authors.initials: L
authors.lastname: Peng
authors.forename: Miaomiao
authors.initials: M
authors.lastname: Song
authors.forename: Qin
authors.initials: Q
authors.lastname: Wu
authors.forename: Guodong
authors.initials: G
authors.lastname: Li
authors.forename: Shangdong
authors.initials: S
authors.lastname: Liang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D005455:Fluorescent Antibody Technique; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D058486:Receptors, Purinergic P2X7 / Q000378:metabolism*; D017783:Superior Cervical Ganglion / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology*
chemical_list: D058486:Receptors, Purinergic P2X7