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Endothelial Dysfunction after Angioplasty: A Pathway for Remodelling?

  • Chapter
Arterial Remodeling: A Critical Factor in Restenosis

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 198))

  • 63 Accesses

Abstract

The endothelium can elicit relaxations when stimulated by neurotransmitters, hormones, substances derived from platelets and the coagulation system (Fig. 1) (1, 2). Furthermore, shear forces exerted by the circulating blood induce endothelium-dependent vasodilation, an important adaptive response of the vasculature during exercise. The mediator of these responses is a diffusible substance with a half-life of a few seconds, the so-called endothelium-derived relaxing factor (EDRF) (2) which has recently been identified as the free radical nitric oxide (NO) (3). Nitric oxide is formed from L-arginine by oxidation of its guanidine-nitrogen terminal (3). The intracellular mechanism by which nitric oxide causes relaxation in vascular smooth muscle cells involves formation of cyclic 3’5’-guanosine monophosphate via the enzyme soluble guanylyl cyclase (Fig. 1) (10).

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Authors and Affiliations

  1. Cardiology, Cardiovascular Research, University Hospital, Bern, Switzerland

    Thomas F. Lüscher & Georg Noll

  2. INSERM Unit 141, Lariboisière Hospital, Paris, France

    Chantal M. Boulanger

Authors
  1. Thomas F. Lüscher
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  2. Georg Noll
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  3. Chantal M. Boulanger
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Editors and Affiliations

  1. Necker University, Paris, France

    Antoine Lafont

  2. Cleveland Clinic Foundation, Cleveland, Ohio, USA

    Eric J. Topol

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© 1997 Springer Science+Business Media New York

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Lüscher, T.F., Noll, G., Boulanger, C.M. (1997). Endothelial Dysfunction after Angioplasty: A Pathway for Remodelling?. In: Lafont, A., Topol, E.J. (eds) Arterial Remodeling: A Critical Factor in Restenosis. Developments in Cardiovascular Medicine, vol 198. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-6079-1_12

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  • DOI: https://doi.org/10.1007/978-1-4615-6079-1_12

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