Document Detail


Adrenal GRK2 lowering is an underlying mechanism for the beneficial sympathetic effects of exercise training in heart failure.
MedLine Citation:
PMID:  20304818     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Exercise training has been reported to exert beneficial effects on cardiac function and to reduce morbidity and mortality of chronic heart failure (HF). Augmented sympathetic nervous system (SNS) activity, leading to elevated circulating catecholamine (CA) levels, is a hallmark of chronic HF that significantly aggravates this disease. Exercise training has been shown to also reduce SNS overactivity in HF, but the underlying molecular mechanism(s) remain unidentified. We recently reported that adrenal G protein-coupled receptor kinase-2 (GRK2), an enzyme that regulates the sympathoinhibitory alpha(2)-adrenoceptors (alpha(2)-ARs) present in the CA-producing adrenal medulla, is upregulated in HF, contributing to the chronically elevated CA levels and SNS activity of the disease. In the present study, we tested whether exercise training can affect the adrenal GRK2-alpha(2)-AR-CA production system in the context of HF. For this purpose, a 10-wk-long exercise training regimen of adult male Sprague-Dawley rats starting at 4 wk postmyocardial infarction (post-MI) was employed, and examination at the end of this treatment period revealed significant amelioration of beta-AR-stimulated contractility in response to exercise training, accompanied by cardiac GRK2 reduction and restoration of circulating plasma CA levels. Importantly, adrenal GRK2 expression (72 + or - 5% reduction vs. post-MI untrained) and alpha(2)-AR number were also restored after exercise training in post-MI animals. These results suggest that exercise training restores the adrenal GRK2-alpha(2)-AR-CA production axis, and this might be part of the mechanism whereby this therapeutic modality normalizes sympathetic overdrive and impedes worsening of the failing heart.
Authors:
Giuseppe Rengo; Dario Leosco; Carmela Zincarelli; Massimo Marchese; Graziamaria Corbi; Daniela Liccardo; Amelia Filippelli; Nicola Ferrara; Michael P Lisanti; Walter J Koch; Anastasios Lymperopoulos
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Publication Detail:
Type:  Journal Article     Date:  2010-03-19
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  298     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-20     Completed Date:  2010-06-23     Revised Date:  2012-06-07    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2032-8     Citation Subset:  IM    
Affiliation:
Cardiology Division, "Salvatore Maugeri" Foundation, IRCCS, Via Bagni Vecchi, 1-82037 Telese Terme, Italy. giuseppe.rengo@unina.it
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MeSH Terms
Descriptor/Qualifier:
Adrenal Medulla / enzymology*
Animals
Catecholamines / blood
Disease Models, Animal
G-Protein-Coupled Receptor Kinase 2 / metabolism*
Heart Failure / metabolism*,  physiopathology*
Male
Myocardial Contraction / physiology
Myocardial Infarction / metabolism,  physiopathology
Physical Conditioning, Animal / physiology*
Rats
Rats, Sprague-Dawley
Receptors, Adrenergic, alpha-2 / metabolism
Sympathetic Nervous System / physiology*
Ventricular Remodeling / physiology
Chemical
Reg. No./Substance:
0/Catecholamines; 0/Receptors, Adrenergic, alpha-2; EC 2.7.11.15/Adrbk1 protein, rat; EC 2.7.11.15/G-Protein-Coupled Receptor Kinase 2

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