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β 2 ‐ but not β 1 ‐adrenoceptor activation modulates intracellular oxygen availability
Author(s) -
Li Jun,
Yan Biao,
Huo Zhaoxia,
Liu Ying,
Xu Jiahong,
Sun Yunfu,
Liu Yi,
Liang Dandan,
Peng Luying,
Zhang Youyi,
Zhou ZhaoNian,
Shi Jingyi,
Cui Jianmin,
Chen YiHan
Publication year - 2010
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.190900
Subject(s) - intracellular , microbiology and biotechnology , cytosol , nitric oxide , nadph oxidase , reactive oxygen species , ampk , enos , chemistry , mitochondrion , homeostasis , nitric oxide synthase , biology , biochemistry , protein kinase a , endocrinology , phosphorylation , enzyme
β‐Adrenoceptors (β‐ARs) play a critical role in the regulation of cardiovascular function. Intracellular oxygen homeostasis is crucial for the survival of cardiomyocytes. However, it is still unclear whether β‐AR activation can modulate intracellular oxygen. Here we used mitochondrial and cytosolic target Renilla luciferase to detect intracellular oxygen concentration. Pharmacological experiments revealed that β 2 ‐AR activation specifically regulates intracellular oxygen in cardiomyocytes and COS7 cells. This effect was abrogated by inhibitory G protein (G i ) inhibition, endothelial nitric oxide synthase (eNOS) blockade, and NO scavenging, implicating that the β 2 ‐AR–G i –eNOS pathway is involved in this regulation. β 2 ‐AR activation increased the AMP/ATP ratio, AMPK activity, ROS production and prolyl hydroxylase activity. These effects also contribute to the regulation of β 2 ‐AR signalling, thus providing an additional layer of complexity to enforce the specificity of β 1 ‐AR and β 2 ‐AR signalling. Collectively, the study provides novel insight into the modulation of oxygen homeostasis, broadens the scope of β 2 ‐AR function, and may have crucial implications for β 2 ‐AR signalling regulation.