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Physiological regulation of cardiac contractility by endogenous reactive oxygen species
Author(s) -
Perjés Á.,
Kubin A.M.,
Kónyi A.,
Szabados S.,
Cziráki A.,
Skoumal R.,
Ruskoaho H.,
Szokodi I.
Publication year - 2012
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2012.02391.x
Subject(s) - contractility , reactive oxygen species , inotrope , microbiology and biotechnology , heart failure , endogeny , mitochondrion , biology , cardiac function curve , medicine , chemistry , endocrinology
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.