Clin Exp Emerg Med.
2016 Sep;3(3):175-180. 10.15441/ceem.16.141.
Cardiac physiologic regulation of sub-type specific adrenergic receptors in transgenic mice overexpressing βâ‚- and β₂-adrenergic receptors
- Affiliations
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- 1Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, Korea.
- 2Department of Emergency Medicine, Kangwon National University School of Medicine, Chuncheon, Korea. cjhemd@kangwon.ac.kr
- 3Bio-Safety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Korea.
- 4CardioPulmonary Genomics Program, Departments of Medicine and Physiology, University of Maryland School of Medicine, Baltimore, MD, USA.
- 5Department of Neurobiology, Kangwon National University School of Medicine, Chuncheon, Korea. mhwon@kangwon.ac.kr
- KMID: 2361024
- DOI: http://doi.org/10.15441/ceem.16.141
Abstract
OBJECTIVE
Combination of βâ‚-adrenergic receptor (AR) blockade and β₂-AR activation might be a potential novel therapy for treating heart failure. However, use of β-AR agonists and/or antagonists in the clinical setting is controversial because of the lack of information on cardiac inotropic or chronotropic regulation by AR signaling.
METHODS
In this study, we performed hemodynamic evaluation by examining force frequency response (FFR), Frank-Starling relationship, and response to a non-selective β-AR agonist (isoproterenol) in hearts isolated from 6-month-old transgenic (TG) mice overexpressing βâ‚- and β₂-ARs (βâ‚- and β₂-AR TG mice, respectively).
RESULTS
Cardiac physiologic consequences of βâ‚- and β₂-AR overexpression resulted in similar maximal response to isoproterenol and faster temporary decline of positive inotropic response in β₂-AR TG mice. βâ‚-AR TG mice showed a pronounced negative limb of FFR, whereas β₂-AR TG mice showed high stimulation frequencies with low contractile depression during FFR. In contrast, Frank-Starling relationship was equally enhanced in both βâ‚- and β₂-AR TG mice.
CONCLUSION
Hemodynamic evaluation performed in the present showed a difference in βâ‚- and β₂-AR signaling, which may be due to the difference in the desensitization of βâ‚- and β₂-ARs.
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