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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Liccardo, D. De Lucia, C. Gargiulo, P. Zincarelli, C. Ferrara, N. Koch, Wj Lymperopoulos, A. Pagano, G. Leosco, D. Rengo, G. Cannavo, A. Femminella, Gd Perrone Filardi, P. |
| Description | Author Affiliation: Rengo G ( Cardiology Division, Fondazione Salvatore Maugeri, IRCCS, Telese Terme (BN), Italy. giuseppe.rengo@unina.it) |
| Abstract | BACKGROUND AND PURPOSE: Sympathetic nervous system (SNS) hyperactivity is characteristic of chronic heart failure (HF) and significantly worsens prognosis. The success of ß-adrenoceptor antagonist (ß-blockers) therapy in HF is primarily attributed to protection of the heart from the noxious effects of augmented catecholamine levels. ß-Blockers have been shown to reduce SNS hyperactivity in HF, but the underlying molecular mechanisms are not understood. The GPCR kinase-2 (GRK2)- (2) adrenoceptor-catecholamine production axis is up-regulated in the adrenal medulla during HF causing (2) -adrenoceptor dysfunction and elevated catecholamine levels. Here, we sought to investigate if ß-blocker treatment in HF could lower SNS activation by directly altering adrenal GRK2 levels. EXPERIMENTAL APPROACH: Four weeks after myocardial infarction-induced HF, adult rats were randomized to 10-week treatment with vehicle (HF/C) or bisoprolol (HF/B). Cardiac function and dimensions were measured. In heart and adrenal gland, GRK2 levels were assessed by RT-PCR and Western blotting and adrenoceptors studied with radioligand binding. Catecholamines and (2) adrenoceptors in adrenal medulla chromaffin cell cultures were also measured. KEY RESULTS: Bisoprolol treatment ameliorated HF-related adverse cardiac remodelling and reduced plasma catecholamine levels, compared with HF/C rats. Bisoprolol also attenuated adrenal GRK2 overexpression as observed in HF/C rats and increased (2) adrenoceptor density. In cultures of adrenal medulla chromaffin cells from all study groups, bisoprolol reversed HF-related (2) adrenoceptor dysfunction. This effect was reversed by GRK2 overexpression. CONCLUSION AND IMPLICATIONS: Blockade of ß-adrenoceptors normalized the adrenal (2) adrenoceptor-catecholamine production axis by reducing GRK2 levels. This effect may contribute significantly to the decrease of HF-related sympathetic overdrive by ß-blockers. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 8 |
| Volume Number | 166 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2012-08-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Adrenergic Beta-Antagonists Pharmacology Bisoprolol Catecholamines Metabolism G-Protein-Coupled Receptor Kinase 2 Heart Failure Receptors, Adrenergic, Alpha-2 Adrenal Glands Cytology Adrenergic Beta-1 Receptor Antagonists Administration & Dosage Animals Cells, Cultured Chromaffin Cells Drug Effects Rats, Sprague-Dawley Genetics Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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