© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Platelets, oxidant stress and erectile dysfunction: an hypothesis
aDepartment of Cardiac Surgery, Division of Cardiac, Anaesthetic and Radiological Sciences, Bristol Royal Infirmary, Bristol BS2 8HW, UK
bDepartment of Urology, Royal Free Hospital and School of Medicine, London, UK
cDepartment of Chemical Pathology, Royal Free Hospital and School of Medicine, London, UK
dDepartment of Biochemistry, Royal Free Hospital and School of Medicine, London, UK
eDepartment of Biomedical Sciences, University of Bradford, Bradford, West Yorkshire, UK
* Corresponding author. Tel.: +44-117-928-3154; fax: +44-117-929-9737 j.y.jeremy@bristol.ac.uk
Received 15 September 1999; accepted 16 December 1999
KEYWORDS Nitric oxide; Leukocytes; Platelets; Smooth muscle
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1 Introduction |
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The successful use of sildenafil (ViagraTM) to treat vasculogenic erectile dysfunction (VED) has heightened awareness of the widespread prevalence of this disorder [1–3]. Sildenafil acts through the augmentation of nitric oxide (NO) actions on vascular/corpus cavernosal smooth muscle cell relaxation [1–4] (Fig. 1). Thus, the therapeutic use of sildenafil has also highlighted the central role played by NO in mediating normal erection and in the pathogenesis of VED. Nevertheless, we still know little about the basic pathophysiology of VED. Since prevention is preferable to cure, it is imperative to improve our understanding of the pathophysiology of VED. In this brief review, we suggest that another major consequence of diminished NO formation is the increased adhesion of platelets and leukocytes, in particular neutrophils, which may counter erection through release of vasconstrictors, superoxide and other oxygen free radicals. We also suggest that erection itself may trigger events that
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2 Erectile dysfunction, vascular disease and oxidant stress |
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3 Platelet–neutrophil interactions |
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4 Therapeutic strategies for reducing erectile dysfunction in the long-term |
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5 Concluding remarks |
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