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Cardiovascular Research 2006 69(2):304-306; doi:10.1016/j.cardiores.2005.12.008
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Copyright © 2005, European Society of Cardiology

The role of cardiac myosin binding protein-C as a regulator of myofilament Ca2+ sensitivity

Harald Kögler*

Herzzentrum Göttingen, Kardiologie und Pneumologie, Georg-August-Universität, Göttingen, Germany

* Heart Center Göttingen, Department of Cardiology, Robert-Koch-Str. 40, 37075 Göttingen, Germany. Tel.: +49 551 396380; fax: +49 551 392953. Email address: hkogler@med.uni-goettingen.de

Received 29 November 2005; accepted 8 December 2005

The first 10% of the full text of this article appears below.

Stimulation of β1-adrenergic receptors in the heart by endogenous or exogenous agonists results in enhanced formation of the second messenger cyclic 3',5'-adenosine monophosphate (cAMP), which in turn activates cAMP-dependent protein kinase (PKA). PKA-catalysed phosphorylation ultimately triggers a variety of target proteins to undergo orchestrated functional changes that together comprise the positive inotropic and lusitropic effects caused by β1-adrenoceptor activation. Both these effects serve to enhance cardiac output: the positive inotropic effect boosts myocyte contractility by optimizing Ca2+ homeostasis, mainly via phosphorylation of phospholamban, sarcoplasmic reticulum (SR) Ca2+-ATPase, and L-type Ca2+ channels. The positive lusitropic effect, on the other hand, accelerates myocyte relaxation, thereby facilitating . . . [Full Text of this Article]


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