Title | Adrenal beta-arrestin 1 promotes physiological aldosterone production | ||
Authors | A. Lymperopoulos and W.J. Koch
Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA, 19107 |
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Citation | Lymperopoulos, A., Koch, W.J.: Adrenal beta-arrestin 1 promotes physiological aldosterone production, Epitheorese Klin. Farmakol. Farmakokinet. 22(2): 224-226 (2008) | ||
Publication Date | 23-25 May 2008 | ||
Full Text Language | English | ||
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Keywords | Beta-arrestin, aldosterone production. | ||
Other Terms | Review article | ||
Summary | Elevated aldosterone levels accompany and aggravate chronic heart failure (HF). Aldosterone is produced by adrenocortical zona glomerulosa (AZG) cells after angiotensin II (AngII) activation of AngII type 1 receptors (AT1Rs), G protein coupled receptors (GPCRs) that also signal independently of G-proteins. This G protein-independent signaling is promoted by βarrestin (βarr) -1 and -2, originally discovered as GPCR signaling terminators. We report here that βarr1 promotes physiological aldosterone production in vivo, in normal rats. These findings suggest adrenal βarr1 inhibition might be of therapeutic value for curbing HF-related hyperaldosteronism. | ||
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Online ISSN 1011-6575
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Articles published in this Journal are Indexed or Abstracted in: • Chemical Abstracts • Elsevier’s Bibliographic Databases: Scopus, EMBASE, EMBiology, Elsevier BIOBASE SCImago Journal and Country Rank Factor
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