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Beta-adrenergic stimulation and myocardial function in the failing heart.

Authors: El-Armouche, A  Eschenhagen, T 
Citation: El-Armouche A and Eschenhagen T, Heart Fail Rev. 2009 Dec;14(4):225-41.
Pubmed: (View Article at PubMed) PMID:19110970
DOI: Full-text: DOI:10.1007/s10741-008-9132-8

The sympathetic nervous system provides the most powerful stimulation of cardiac function, brought about via norepinephrine and epinephrine and their postsynaptic beta-adrenergic receptors. More than 30 years after the first use of practolol in patients with heart failure beta blockers are now the mainstay of the pharmacological treatment of chronic heart failure. Many aspects of their mechanism of action are well understood, but others remain unresolved. This review focuses on a number of questions that are key to further developments in the field. What accounts for and what is the role of beta-adrenergic desensitization, a hallmark of the failing heart? Is part of this adaptation predominantly beneficial and should therefore be reinforced, another part mainly maladaptive and therefore a target for antagonists? Which lessons can be drawn from studies in genetically engineered mice, which from (pharmaco) genetic studies? Finally, what are promising targets downstream of beta-adrenergic receptors that go beyond the current neurohumoral blockade?


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RGD Object Information
RGD ID: 4140391
Created: 2010-08-25
Species: All species
Last Modified: 2010-08-25
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.