Platelet Nitric Oxide Signaling System in Patients with Coronary Artery Disease

Abstract

Coronary artery disease (CAD) is the leading cause of death worldwide, and the major cause of hospital admissions in the Western countries. The pathogenesis of CAD is closely related to nitric oxide release and formation. The purpose of this study was to investigate the status of platelets nitric oxide in patients with coronary artery disease. We measured platelets aggregation, cGMP, NO (nitrite/nitrate level), NO synthase activity, plasma NO, and ionized Ca(2+) in 40 healthy volunteers and 120 patients with myocardial infarction, unstable and stable angina, with 40 subjects in each group. The subjects' age mean range was from 40-51 years. Platelets aggregation, NO, cGMP, NO synthase activity, plasma NO and ionized Ca(2+) have increased significantly (P <0.001) across the patients groups compared to controls. Platelets NO synthase activity (mean ± SD / U / 10(9) platelets) in healthy controls, MI, unstable angina and stable angina patients were 1.19 ± 0.56, 1.21 ± 0.64, 1.64 ± 0.98 and 1.57 ± 0.81 respectively. The cGMP (mean ± SD / pmole / 10(9) platelets) levels were 0.95 ± 0.41, 1.53 ± 0.64, 3.18 ± 0.77, and 5.12 ± 1.5 respectively. The present study demonstrated that platelets aggregation, NO, cGMP, NO synthase activity, plasma NO, and ionized Ca(2+) profoundly increased in CAD. The increases in NO-cGMP components may have resulted as a compensatory response to ameliorate platelet activity and Ca(2+) levels in CAD patients.