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.

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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