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Involvement of NADPH oxidase in coronary flow regulation by adeno | 54652
Clinical & Experimental Cardiology

Clinical & Experimental Cardiology
Open Access

ISSN: 2155-9880

+44 1300 500008

Involvement of NADPH oxidase in coronary flow regulation by adenosine receptors


14th International Conference on Clinical & Experimental Cardiology

November 14-16, 2016 Orlando, Florida, USA

S Jamal Mustafa

West Virginia University, USA

Scientific Tracks Abstracts: J Clin Exp Cardiolog

Abstract :

Adenosine increases Coronary Flow (CF) through the activation of A2A and A2B Adenosine Receptors (ARs). However, these mechanisms are not fully understood. We previously showed that adenosine-induced increase in CF is in part through NADPH oxidase (Nox), which is independent of A1 or A3 ARs. In this study, we hypothesize that adenosine-mediated increase in CF is through Nox activation and depends on A2A but not on A2B ARs. Functional studies were conducted using Langendorff mouse hearts. Hydrogen peroxide (H2O2) production was measured in isolated coronary arteries from WT, A2A and A2BAR KO mice using immunofluorescence. Adenosine-induced concentration-dependent increase in CF was attenuated by the specific Nox2 inhibitor gp91 ds-tat or reactive oxygen species (ROS) scavenger EUK134 in both WT and A2B but not A2A AR KO hearts. Similarly, the A2A AR selective agonist CGS-21680-induced increase in CF was significantly blunted by Nox2 inhibition in both WT and A2B AR KO, while the A2B AR selective agonist BAY 60-6583-induced increase in CF was not affected by Nox2 inhibition in WT. In intact isolated coronary arteries, adenosine-induced (10�?¼M) increase in H2O2 formation in both WTand A2BAR KO mice was attenuated byNox2 inhibition, whereas adenosine failed to increase H2O2 production in A2A AR KO mice. In conclusion, adenosine-induced increase in CF is partially mediated by Nox2-derived H2O2, which critically depends upon the presence of A2A AR. These studies may lead to better understanding of the role of ARs in coronary disease and may lead to better therapeutic approaches.

Biography :

S Jamal Mustafa is a Professor of Physiology and Pharmacology at West Virginia University (WVU). He received Dean’s Award for Excellence in Research from SOM in 2008 and became a Robert C Byrd Professor in 2010 and received Chancellor’s Award for Outstanding Achievement in Research and Scholarly Activities from HSC in 2013. He has published over 200 manuscripts. Our past work has led to the approval of an A2A selective AR agonist (Lexican®) for myocardial perfusion imaging. Currently, we are using AR and β adrenergic receptor KOs to better understand the relationship between these receptors in coronary flow regulation.

Email: sjmustafa@hsc.wvu.edu

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