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Updated: Oct 4, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Mitochondrial K(ATP) channel opening protects a human atrial-derived cell line by a mechanism involving free radical

R Carroll1, V A Gant, D M Yellon

  • 1The Hatter Institute and Centre for Cardiology, University College Hospital and Medical School, Grafton Way, London WC1E 6DB, UK. hatter-institute@ucl.ac.uk

Cardiovascular Research
|September 1, 2001
PubMed
Abstract

Insights

Mitochondrial K(ATP) channel openers, like diazoxide, may trigger preconditioning. This study shows diazoxide triggers protection via mitochondrial swelling and reactive oxygen species (ROS) generation in simulated ischemia/reperfusion.

Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Cellular Physiology

Background:

  • The protective mechanisms of mitochondrial K(ATP) channel openers against ischemia/reperfusion (I/R) injury are not fully understood.
  • Emerging evidence suggests these openers may act as triggers rather than solely effectors.

Purpose of the Study:

  • To investigate the role of the mitochondrial K(ATP) channel opener, diazoxide, in simulated ischemia/reperfusion (sI/R) injury.
  • To examine the effects of diazoxide on mitochondrial function, specifically reactive oxygen species (ROS) generation.

Main Methods:

  • Utilized a human atrial-derived cell line model of simulated ischemia/reperfusion (sI/R).
  • Assessed cell survival using propidium iodide (PI) exclusion.
  • Measured ROS generation using a specific probe and mitochondrial membrane potential with JC-1.

Main Results:

  • Diazoxide conferred significant protection against sI/R-induced cell death.
  • This protection was abolished by the mitoK(ATP) channel blocker 5-hydroxydecanoate (5-HD) and the ROS scavenger 2-mercaptopropionylglycine (MPG).
  • Diazoxide increased ROS generation and induced mitochondrial swelling, without altering mitochondrial membrane potential.

Conclusions:

  • Diazoxide acts as a trigger for preconditioning in this model.
  • The mechanism involves mitochondrial swelling and ROS generation.
  • These findings provide novel insights into the protective effects of mitoK(ATP) channel openers.

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