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Mitochondrial pores modulate the protective effect of acetylcholine on ventricular myocytes during

Guo-Quan Sun1, Jue Wang, Qing Li

  • 1Department of Physiology, Zhejiang Medical College, Hangzhou, China.

Methods and Findings in Experimental and Clinical Pharmacology
|April 20, 2010
PubMed

Insights

Acetylcholine (ACh) protects heart cells from injury by activating the mitochondrial ATP-sensitive potassium channel (mitoK(ATP) channel). This action inhibits the mitochondrial permeability transition pore (MPTP) opening, preserving cell function during ischemia-reperfusion.

Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Cellular Physiology

Background:

  • Ischemia-reperfusion (I/R) injury is a significant cause of heart damage.
  • Mitochondrial dysfunction, including MPTP opening, plays a key role in I/R injury.
  • The role of acetylcholine (ACh) in mitigating I/R injury via specific mitochondrial pathways requires further elucidation.

Purpose of the Study:

  • To investigate the cardioprotective effects of acetylcholine (ACh).
  • To determine if ACh modulates mitochondrial permeability transition pore (MPTP) opening through the mitochondrial ATP-sensitive potassium channel (mitoK(ATP) channel) during ischemia-reperfusion (I/R).

Main Methods:

  • Isolated rat ventricular myocytes were subjected to simulated ischemia and reperfusion (I/R).
  • Acetylcholine (ACh) was administered prior to I/R.
  • MitoK(ATP) channel inhibition (5-hydroxydecanoate, 5-HD) and MPTP opening (atractyloside, Atr) were used to probe mechanisms.
  • Myocyte contractile function, viability, LDH release, ROS, and mitochondrial membrane potential were assessed.

Main Results:

  • ACh pretreatment improved myocyte contractile function and viability during I/R.
  • ACh significantly reduced I/R-induced cell death, LDH release, ROS generation, and mitochondrial membrane potential dissipation.
  • The protective effects of ACh were abolished by the mitoK(ATP) inhibitor (5-HD) and the MPTP opener (Atr).

Conclusions:

  • Acetylcholine (ACh) exerts cardioprotective effects against ischemia-reperfusion (I/R) injury.
  • ACh protects ventricular myocytes by inhibiting MPTP opening and stabilizing mitochondrial membrane potential.
  • These protective mechanisms are mediated through the activation of the mitoK(ATP) channel.

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