Whole body nitric oxide production is not decreased in patients with coronary atherosclerosis but is inversely related to plasma homocysteine

  • Peter D. O’Kane
    Department of Cardiology, Cardiothoracic Centre, St Thomas’ Hospital, London, UK

    Department of Clinical Pharmacology, Cardiovascular Division, King's College London, London, UK
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  • Graham Jackson
    Department of Cardiology, Cardiothoracic Centre, St Thomas’ Hospital, London, UK
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  • Albert Ferro
    Corresponding author at: Department of Clinical Pharmacology, King's College London, Room 3.07 Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK. Tel.: +44 20 7848 4283; fax: +44 20 7848 4500.
    Department of Clinical Pharmacology, Cardiovascular Division, King's College London, London, UK
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      Vascular endothelial nitric oxide (NO) biosynthesis is reported to be decreased in patients with atherosclerosis. The primary aim of the present study was to determine whether whole body NO production is decreased in patients with established coronary atherosclerosis (CA) as compared to healthy control (HC) subjects. As a secondary aim, we wished to ascertain whether whole body NO biosynthesis is inversely related to plasma homocysteine (Hcy) levels.


      Whole body NO production was assessed by measuring the amount of [15N]-nitrate excreted in urine, following intravenous administration of l-[15N]2-arginine.


      19 CA and 13 HC.


      Mean urinary [15N]-nitrate excretion was not different between the CA (113.1 ± 13.9 nmol/mmol creatinine) and HC (129.9 ± 15.4 nmol/mmol creatinine) groups, and was not different in CA subjects taking nitrates as compared to those not taking nitrates. Linear regression analysis revealed a strong inverse correlation between [15N]-nitrate excretion and plasma Hcy concentration (r = 0.475, p = 0.012). In contrast, no relationship was observed between [15N]-nitrate excretion and age, blood pressure (systolic or diastolic), plasma cholesterol (including subfractions), triglycerides or glucose.


      Whole body NO production is inversely related to plasma Hcy, but is not related either to established coronary atherosclerosis or to the presence of other cardiovascular risk factors.


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