Circulation Research. 2003;93:896-906
doi: 10.1161/01.RES.0000102042.83024.CA
doi: 10.1161/01.RES.0000102042.83024.CA
© 2003 American Heart Association, Inc.
Reviews |
What Is the Role of ß-Adrenergic Signaling in Heart Failure?
From the Institute of Pharmacology (M.J.L., S.E.), Wuerzburg, Germany; Institute of Experimental and Clinical Pharmacology (T.E.), Universitaetsklinikum Hamburg-Eppendorf, Germany.
Correspondence to Martin Lohse, Institute of Pharmacology, Versbacher Straße 9, 97078 Wuerzburg, Germany. E-mail lohse{at}toxi.uni-wuerzburg.de
Steven Houser Guest Editor
This Review is part of a thematic series on Unanswered Questions in Heart Failure, which includes the following articles:
Is Depressed Myocyte Contractility Centrally Involved in Heart Failure?
What Is the Role of ß-Adrenergic Signaling in Heart Failure?
What Causes Sudden Death in Heart Failure?
Is Abnormal Cell Growth and Hypertrophy the Cause of Heart Failure?
Does Energy Starvation Cause Heart Failure?
What Mechanisms Underlie Diastolic Dysfunction in Heart Failure?
This review addresses open questions about the role of ß-adrenergic receptors in cardiac function and failure. Cardiomyocytes express all three ß-adrenergic receptor subtypes—ß1, ß2, and, at least in some species, ß3. The ß1 subtype is the most prominent one and is mainly responsible for positive chronotropic and inotropic effects of catecholamines. The ß2 subtype also increases cardiac function, but its ability to activate nonclassical signaling pathways suggests a function distinct from the ß1 subtype. In heart failure, the sympathetic system is activated, cardiac ß-receptor number and function are decreased, and downstream mechanisms are altered. However, in spite of a wealth of data, we still do not know whether and to what extent these alterations are adaptive/protective or detrimental, or both. Clinically, ß-adrenergic antagonists represent the most important advance in heart failure therapy, but it is still debated whether they act by blocking or by resensitizing the ß-adrenergic receptor system. Newer experimental therapeutic strategies aim at the receptor desensitization machinery and at downstream signaling steps.
Key Words: ß-adrenergic receptors • G proteins • transgenic mice • cardiac hypertrophy • apoptosis
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A. Morimoto, H. Hasegawa, H.-J. Cheng, W. C. Little, and C.-P. Cheng Endogenous {beta}3-adrenoreceptor activation contributes to left ventricular and cardiomyocyte dysfunction in heart failure Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2425 - H2433. [Abstract] [Full Text] [PDF]
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S. Engelhardt, L. Hein, V. Dyachenkow, E. G. Kranias, G. Isenberg, and M. J. Lohse Altered Calcium Handling Is Critically Involved in the Cardiotoxic Effects of Chronic {beta}-Adrenergic Stimulation Circulation, March 9, 2004; 109(9): 1154 - 1160. [Abstract] [Full Text] [PDF]
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