Physiological regulation of cardiac contractility by endogenous reactive oxygen species

A. Perjés, A. M. Kubin, A. Kónyi, S. Szabados, A. Cziráki, R. Skoumal, H. Ruskoaho, I. Szokodi

Research output: Contribution to journalReview article

19 Citations (Scopus)


Increased production of reactive oxygen species (ROS) has been linked to the pathogenesis of congestive heart failure. However, emerging evidence suggests the involvement of ROS in the regulation of various physiological cellular processes in the myocardium. In this review, we summarize the latest findings regarding the role of ROS in the acute regulation of cardiac contractility. We discuss ROS-dependent modulation of the inotropic responses to G protein-coupled receptor agonists (e.g. β-adrenergic receptor agonists and endothelin-1), the potential cellular sources of ROS (e.g. NAD(P)H oxidases and mitochondria) and the proposed end-targets and signalling pathways by which ROS affect contractility. Accumulating new data supports the fundamental role of endogenously generated ROS to regulate cardiac function under physiological conditions.

Original languageEnglish
Pages (from-to)26-40
Number of pages15
JournalActa Physiologica
Issue number1
Publication statusPublished - May 1 2012


  • Beta adrenergic
  • Cardiac contractility
  • Endothelin
  • Reactive oxygen species
  • Signal transduction

ASJC Scopus subject areas

  • Physiology

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