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Editorial
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This editorial highlights the critical role of endothelial nitric oxide (NO) in vascular homeostasis and how its deficiency contributes to various cardiovascular diseases.
See doi:10.1016/j.ehj.2003.08.013 for the article to which this editorial refers The endothelium is one of the biggest organ systems in our body. This is not so apparent on first view, as it is spread throughout the body mostly in tiny arterioles and capillaries. If you should be asked to define the endothelium's ‘personality’, you would certainly come to the notion that this organ is characterized by a negative attitude: If vasoconstrictors attempt to constrict our arteries, the endothelium says ‘NO’; if platelets tend to adhere to the vessel wall, the endothelium says NO’; if monocytes try to invade the vascular wall by penetrating the endothelial lining, the endothelium says ‘NO’ again; finally, if oxygen radicals sound the charge against the vasculature, it is the endothelium once more that sends out a burst of ‘NO's to neutralize the offense.1 In the belligerently sounding setting of what we use to call ‘vascular homeostasis’, the endothelium with its major mediator, nitric oxide (NO) is one of the most valuable protective factors. It is a lack of NO or a deficiency of NO's actions in the vascular wall that lies behind most of the cardiovascular diseases that we face today: coronary heart disease, hypertension, chronic heart failure, vasculopathies associated with diabetes mellitus, hyperhomocysteinemia, and atherosclerosis in general, to name the best known among them.
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Rainer H. Böger (2003) studied this question.
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