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Aspirin and endothelial function in hypertension

Journal of Human Hypertension volume 19, pages 663–665 (2005)Cite this article

Hypertension is associated with the flow of blood under high pressure, and yet the complications of hypertension, such as myocardial infarction or stroke are, paradoxically, thrombotic rather than haemorrhagic — the so-called ‘thrombotic paradox of hypertension’ (or ‘Birmingham paradox’).1 Increasing evidence also shows that hypertension fulfils the prerequisites of the Virchow's triad for thrombogenesis, with abnormalities in platelets and clotting factors, leading to a prothrombotic or hypercoagulable state. The endothelium is central to the interactions between thrombogenesis and atherogenesis in vascular disease,2 which may involve additional pathophysiological processes, such as angiogenesis.3

The vascular endothelium is essential for vascular homeostasis by releasing a diversity of paracrine and autocrine substances.4 Importantly, a healthy endothelium promotes vasodilatation and inhibits inflammation, platelet aggregation / adhesion and vascular smooth muscle cell proliferation, and thereby exhibits antiatherogenic effects.5, 6 These biological actions, which are largely mediated by the release of nitric oxide (NO), make the endothelium an important component in the endogenous defence against atherosclerosis and its overt clinical complications. Conversely, the loss of the functional integrity of the endothelium, as commonly seen in the environment of cardiovascular risk factors (such as diabetes, hypertension, hypercholesterolaemia, etc), plays an integral role in all stages of atherosclerosis from lesion initiation to plaque rupture.7

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Authors and Affiliations

  1. University Department of Medicine, Haemostasis, Thrombosis and Vascular Biology Unit, City Hospital, Birmingham, England, UK

    D Felmeden, S K Nadar & G Y H Lip

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  1. D Felmeden
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  2. S K Nadar
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Correspondence to G Y H Lip.

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Felmeden, D., Nadar, S. & Lip, G. Aspirin and endothelial function in hypertension. J Hum Hypertens 19, 663–665 (2005). https://doi.org/10.1038/sj.jhh.1001880

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