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Angiology
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Effect of Cardiovascular Drugs on Adenosine Deaminase Activity

Edward Kowalczyk, PhD

Department of Pharmacology

Maria Kopff, PhD

Department of Chemistry and Clinical Biochemistry

Jan Kowalski, PhD

Department of Internal Diseases and Cardiological Rehabilitation

Anna Kopff, PhD

Dimitri P. Mikhailidis, MD, BSc

Department of Clinical Biochemistry (Vascular Disease Prevention Clinics), Royal Free Hospital Campus, University College London (UCL), London

Marcin Barylski, PhD

Department of Cardiology, 1st Chair of Cardiology and Cardiac Surgery Medical University of Lodz, Poland

Maciej Banach, PhD

Department of Molecular Cardionephrology and Hypertension, Medical University of Lodz, Zeromskiego 113; 90-549 Lodz, Poland, maciejbanach{at}aol.co.uk

Objective: Adenosine deaminase catalyzes the conversion of adenosine and deoxyadenosine to inosine and deoxyinosine, respectively. Because raising adenosine concentration can affect several physiological processes we studied the effect of a selection of cardiological drugs on adenosine deaminase activity in red blood cells and rabbit plasma after 21 days administration. Methods and Results: We determined the activity of adenosine deaminase isoenzymes (ADA1 and ADA2). Simvastatin, aspirin, metoprolol, and isosorbide mononitrate significantly decreased plasma total adenosine activity (by 50%, 34%, 29%, and 19%, respectively; P < .05 to P < .001) mainly by decreasing the activity of ADA2. Conclusions: As a consequence of decreased ADA2 activity , the half-life of adenosine will be lengthened. This may, at least in part, explain some of the beneficial effects of analyzed drugs. Our results might be clinically relevant in patients with coronary artery disease, acute coronary syndromes, heart failure, or stroke where the investigated drugs are commonly used. However, our results should be confirmed in large studies in humans.

Key Words: adenosine deaminase • simvastatin • aspirin • metoprolol and isosorbide mononitrate • molsidomine • isoenzymes

This version was published on January 1, 2009

Angiology, Vol. 59, No. 6, 740-744 (2009)
DOI: 10.1177/0003319708323495
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