Enhanced Expression of β3-Adrenoceptors in Cardiac Myocytes Attenuates Neurohormone-Induced Hypertrophic Remodeling Through Nitric Oxide Synthase
Author(s) -
Catharina Belge,
Joanna Hammond,
Emilie DuboisDeruy,
Boris Manoury,
Julien Hamelet,
Christophe Beauloye,
Andreas Markl,
AnneCatherine Pouleur,
Luc Bertrand,
Hrag Esfahani,
Karima Jnaoui,
Konrad R. Götz,
Viacheslav O. Nikolaev,
Annelies Vanderper,
Paul Herijgers,
Irina Lobysheva,
Guido Iaccarino,
Denise HilfikerKleiner,
Geneviève Tavernier,
Dominique Langin,
Chantal Dessy,
JeanLuc Balligand
Publication year - 2013
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.113.004940
Subject(s) - medicine , phenylephrine , endocrinology , nitric oxide synthase , muscle hypertrophy , myocyte , angiotensin ii , endothelial nos , nitric oxide , fibrosis , receptor , enos , blood pressure
β1-2-adrenergic receptors (AR) are key regulators of cardiac contractility and remodeling in response to catecholamines. β3-AR expression is enhanced in diseased human myocardium, but its impact on remodeling is unknown.
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