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Cardiovascular Research 2001 52(1):161-163; doi:10.1016/S0008-6363(01)00413-8
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Endothelin receptor blockade and nitric oxide bioactivity

[Cardiovascular Research 2001;49:146–151]

Matthias Barton* and Bernhard Glodny

Medical Policlinic and Clinical Atherosclerosis Research Laboratory, Department of Internal Medicine, University Hospital, Rämistrasse 100, CH-8091 Zürich, Switzerland

* Corresponding author. Tel.: +41-1-255-5663, ext. 163105; fax: +41-1-255-8747 bartonm@swissonline.ch

Received 30 May 2001; accepted 18 July 2001

KEYWORDS Acetylcholine; Atherosclerosis; Endothelial function; Endothelins; Nitric oxide

The first 10% of the full text of this article appears below.

In a recent paper, Verma et al. reported abnormal endothelium-dependent relaxation to acetylcholine in isolated internal mammary arteries obtained from patients with coronary artery disease [1]. The authors also observed a moderate increase of the maximum response but not of the sensitivity of these relaxations after 20 min of incubation with micromolar concentrations of either bosentan, a non-selective ET receptor antagonist, BQ-123 (an ETA selective compound) or BQ-788 (an ETB selective compound at low concentrations). The improvement of endothelium-dependent relaxation averaged between 10 and 17% of complete relaxation compared to control experiments, and was not present in endothelium-denuded vessels and not evident in response to the endothelium-independent vasodilator sodium nitroprusside according to the authors’ unpublished data. The authors concluded that both ETA . . . [Full Text of this Article]


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