© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Nitric oxide and coronary endothelial dysfunction in humans
Abteilung Kardiologie, Medizinische Hochschule Hannover, Carl-Neubergstrasse 1, 30625 Hannover, Germany
* Corresponding author. Tel.: +49-511-532-3841; fax: +49-511-532-5412 Drexler.Helmut@MH-Hannover.de
Received 20 January 1999; accepted 9 April 1999
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1 Introduction |
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The endothelium provides a variety of important functions involved in the cardiovascular homeostasis. The assessment of endothelial function in humans has focused primarily on endothelial dependent vasomotion in response to the release of NO. In particular, clinical studies have evaluated vasomotor tone following changes in flow or stimuli for the release of NO from the endothelium, such as acetylcholine, substance P or serotonin [1]. However, NO not only acts as a vasodilating substance but also affects other functions of the endothelium such as the adhesive properties of the endothelium with respect to the interaction with leucocytes and platelets [2]. Despite the pivotal contribution of in vitro studies for the elucidation of underlying mechanisms, the clinical implication of endothelial function can only be appreciated by studies in humans in vivo, since tissue or cells are exposed to an artificial environment i.e. lacking the neurohumoral influences present in vivo. To
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2 Normal endothelial function |
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3 Endothelial function in hypercholesterolemia and arteriosclerosis |
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4 Endothelial function in the coronary micrcocirculation |
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5 Potential mechanisms for the development of endothelial dysfunction |
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6 Functional consequences of impaired NO availability in coronary arteries |
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7 Risk factors and endothelial function |
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8 Effect of cholesterol lowering by statins on endothelial dysfunction |
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9 Inactivation of NO as a cause of endothelial dysfunction |
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10 Peripheral endothelial function as a surrogate for the coronary circulation |
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11 Conclusions |
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