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Physiological regulation of cardiac contractility by endogenous reactive oxygen species

A Perjés1, A M Kubin, A Kónyi

  • 1Heart Institute, Medical School, University of Pécs, Hungary.

Acta Physiologica (Oxford, England)
|April 3, 2012
PubMed

Insights

Reactive oxygen species (ROS) regulate cardiac contractility. This review highlights how ROS, produced by sources like mitochondria, acutely modulate heart muscle function under normal physiological conditions.

Area of Science:

  • Cardiovascular Physiology
  • Oxidative Stress Biology

Background:

  • Increased reactive oxygen species (ROS) production is implicated in heart failure.
  • Emerging evidence points to ROS's role in normal myocardial cellular processes.

Purpose of the Study:

  • To review the role of ROS in the acute regulation of cardiac contractility.
  • To discuss ROS-dependent signaling in response to G protein-coupled receptor agonists.

Main Methods:

  • Literature review of recent findings on ROS and cardiac function.
  • Analysis of cellular sources and signaling pathways of ROS in the heart.

Main Results:

  • ROS acutely regulate cardiac contractility.
  • ROS modulate inotropic responses to agonists like beta-adrenergic receptor agonists.
  • NAD(P)H oxidases and mitochondria are key cellular sources of ROS.

Conclusions:

  • Endogenously generated ROS play a fundamental role in regulating cardiac function physiologically.
  • ROS are critical for the acute regulation of myocardial contractility.

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