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- W2045374311 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 P2X3, P2X2/3 receptors by endogenous ATP contributes to the development of hyperalgesia. The present results have shown that the sensitivity of P2X2/3 receptor in nodose ganglion neurons was increased after myocardial ischemic injury under electrophysiological observation. The inhibitive role of P2X2/3 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 P2X2 and P2X3 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 P2X2/3 receptors in NG neurons was involved in the transmission of myocardial ischemic nociceptive signal." @default.
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- W2045374311 date "2010-12-01" @default.
- W2045374311 modified "2023-10-18" @default.
- W2045374311 title "P2X2/3 receptor activity of rat nodose ganglion neurons contributing to myocardial ischemic nociceptive signaling" @default.
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- W2045374311 doi "https://doi.org/10.1016/j.autneu.2010.06.002" @default.
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