Endothelial Nitric Oxide Synthase – A Target for Stroke Protection by Statins

Author(s): Ulrich Laufs, Matthias Endres

Journal Name: Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Under Re-organization)
(Formerly Current Medicinal Chemistry - Immunology, Endocrine & Metabolic Agents)

Volume 8 , Issue 2 , 2008


Endothelium-derived nitric oxide (eNO) is a central regulator of vascular function and blood flow. eNO is a potent vasodilator, inhibits platelet aggregation and prevents monocytes adhesion. In addition, NO availability is an important determinant of the functional capacity of endothelial progenitor cells and neovascularization. Consequently, eNO plays a central protective role during the pathogenesis of ischaemic stroke. Experimental and clinical studies have demonstrated that statins increase the bio- availability of endothelial NO indirectly via cholesterol-lowering as well as through direct cholesterol-independent mechanisms. On the basis of animal studies and clinical trials, statins have emerged as a potential novel strategy to protect from ischaemic strokes. These data raise the questions whether patients with acute cerebral ischaemia may benefit from intravenous treatment with a statin and, whether these patients are at risk when their ongoing statin treatment is withdrawn.

Keywords: Statins, stroke, endothelium, nitric oxide

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Article Details

Year: 2008
Page: [162 - 166]
Pages: 5
DOI: 10.2174/187152208784587926
Price: $58

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