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Updated: Feb 17, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
P2X7 receptor regulates sympathoexcitatory response in myocardial infarction rats via NF-κB and MAPK pathways
Qin Wu1,2, Hongtao Xu1, Ling Hao1
1Department of Medical Technology, Yancheng Vocational Institute of Health SciencesYancheng, China.
Abstract:
Previous studies have provided evidence for the regulatory effect of P2X7 receptor (P2X7R) on cardiovascular activities. Our study focused on exploring the function and fundamental mechanism of microglial P2X7R in controlling sympathoexcitatory response using rats with acute myocardial infarction (AMI). Coronary artery ligation was used in rats to cause AMI. And before that, rats were administrated with P2X7R siRNA that targeted P2X7R mRNA into paraventricular nucleus (PVN) or BBG (Brilliant Blue G, a P2X7 receptor antagonist). Increased expression levels of P2X7R and adenosine triphosphate (ATP) were observed in the hypothalamic PVN of AMI rats. Moreover, the knockdown of P2X7R expression by P2X7-siRNA or suppression of P2X7 receptor by BBG attenuated the elevation of both vasopressin and oxytocin levels in the PVNs of AMI rats. There was also a decrease in renal sympathetic nerve activity (RSNA) by P2X7-siRNA and BBG. Besides, inflammation was alleviated by P2X7-siRNA and BBG through suppressing pro-inflammatory cytokines IL-1β and IL-6 in PVN of AMI rats. Furthermore, blockade of P2X7R moderated the process of cardiac remodeling. This was achieved due to the regulatory effect of P2X7R on sympathoexcitatory response by influencing NF-κB and mitogen-activated protein kinase (MAPK) signaling. These findings suggest that P2X7R can act as a new regulator of sympathoexcitatory response via NF-κB and MAPK signaling pathways in AMI rats.
Insights
The P2X7 receptor (P2X7R) in the brainstem regulates sympathetic nerve activity and inflammation following heart attack. Blocking P2X7R in rats with myocardial infarction reduced harmful cardiovascular responses.
Area of Science:
- Cardiovascular Physiology
- Neuroimmunology
- Molecular Biology
Background:
- The P2X7 receptor (P2X7R) is implicated in cardiovascular regulation.
- Microglial P2X7R's role in sympathoexcitatory responses during acute myocardial infarction (AMI) requires elucidation.
Purpose of the Study:
- To investigate the mechanism of microglial P2X7R in controlling sympathoexcitatory response in rats with AMI.
- To explore the impact of P2X7R on inflammation and cardiac remodeling post-AMI.
Main Methods:
- Acute myocardial infarction (AMI) induced by coronary artery ligation in rats.
- Administration of P2X7R siRNA or Brilliant Blue G (BBG) into the paraventricular nucleus (PVN).
- Measurement of P2X7R, ATP, vasopressin, oxytocin, renal sympathetic nerve activity (RSNA), inflammatory cytokines (IL-1β, IL-6), and cardiac remodeling markers.
Main Results:
- P2X7R and ATP levels increased in the PVN of AMI rats.
- P2X7R knockdown or blockade attenuated vasopressin and oxytocin levels, decreased RSNA, and reduced IL-1β and IL-6 in the PVN.
- P2X7R blockade mitigated cardiac remodeling by influencing NF-κB and MAPK signaling pathways.
Conclusions:
- Microglial P2X7R plays a critical role in regulating sympathoexcitatory responses in AMI.
- P2X7R influences inflammation and cardiac remodeling via NF-κB and MAPK signaling pathways.
- Targeting P2X7R presents a potential therapeutic strategy for managing AMI complications.
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