Journal
CELLULAR SIGNALLING
Volume 41, Issue -, Pages 33-40Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2017.01.014
Keywords
Nitric oxide; beta-adrenergic receptor; G protein-coupled receptor kinase; Cardiovascular system
Categories
Funding
- NIH [R37 HL061690, NIH P01 HL075443, NIH P01 HL091799, NIH P01 HL108806, NIH R01 HL071818]
Ask authors/readers for more resources
Nitric oxide (NO), initially identified as endothelium-derived relaxing factor (EDRF), is a gaso-transmitter with important regulatory roles in the cardiovascular, nervous and immune systems. In the former, this diatomic molecule and free radical gas controls vascular tone and cardiac mechanics, among others. In the cardiovascular system, it is now understood that p-adrenergic receptor (beta AR) activation is a key modulator of NO generation. Therefore, it is not surprising that the up-regulation of G protein-coupled receptor kinases (GRK5), in particular GRK2, that restrains pAR activity contributes to impaired cardiovascular functions via alteration of NO bioavailability. This review, will explore the specific interrelation between beta ARs, GRK2 and NO in the cardiovascular system and their inter-relationship for the pathogenesis of the onset of disease. Last, we will update the readers on the current status of GRK2 inhibitors as a potential therapeutic strategy for heart failure with an emphasis on their ability of rescuing NO bioavailability. (C) 2017 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available