The role of nitric oxide in A3 adenosine receptor-mediated cardioprotection

• Published in: Autonomic & autacoid pharmacology Vol. 29; no. 3; p. 97
• Main Authors: Hussain, A, Karjian, P, Maddock, H
• Format: Journal Article
• Language: English
• Published: England 01-07-2009
• Subjects: Animals; Cardiotonic Agents - therapeutic use; Coronary Disease - surgery; Coronary Disease - therapy; Female; Humans; Male; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - prevention & control; Nitric Oxide - physiology; Receptor, Adenosine A3 - physiology
• ISSN: 1474-8673
• DOI: 10.1111/j.1474-8673.2009.00438.x

1 Limiting the impact of ischemia reperfusion-related cell death is of vital importance given the enormous figures of heart related mortality in the world. 2 Coronary heart disease (CHD) is responsible for over 100,000 deaths in the UK each year, and is the most common cause of premature death in the UK and as a whole it is estimated that there are just over 1.5 million men, and 1.1 million women, who have suffered CHD in the form of either angina or myocardial infarction (http://www.heartstats.org). 3 In patients undergoing standard clinical reperfusion treatment today such as thrombolysis, percutaneous coronary angioplasty (primary PCTA), and bypass surgery, there remains an underscored need for novel therapies and strategies to reduce post-ischemic infarct size. 4 This review focuses on some of the intracellular signalling pathways that have been proposed to be coupled to A3 adenosine receptors in order to reduce post-ischemic infarct size, in particular the role of nitric oxide in A3 adenosine receptor-mediated cardioprotection is discussed.