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Mitochondrial production of reactive oxygen species contributes to the β‐adrenergic stimulation of mouse cardiomycytes
Author(s) -
Andersson Daniel C.,
Fauconnier Jérémy,
Yamada Takashi,
Lacampagne Alain,
Zhang ShiJin,
Katz Abram,
Westerblad Håkan
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.202838
Subject(s) - reactive oxygen species , stimulation , intracellular , microbiology and biotechnology , receptor , contraction (grammar) , mitochondrion , heart failure , cell , chemistry , adrenergic receptor , medicine , biology , endocrinology , biophysics , biochemistry
Non‐technical summary  When under stress, the heart beat becomes stronger, in part due to enhanced fluxes of Ca 2+ at the level of the cardiac cell. It is known that this effect is mediated by activation of β‐receptors on the cardiac cell surface. This leads to modifications of intracellular proteins that in turn increase the flux of Ca 2+ within the cell. In this study we show that activation of β‐receptors increases the production of reactive oxygen species (ROS) in the heart cell. These ROS generate enhanced Ca 2+ fluxes and more vigorous contraction. This finding shows a new cellular signalling route for regulating the power of the heart beat and might contribute to our understanding of diseases with defective cardiac contraction, such as heart failure.

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