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Cardiovascular Research 2004 61(4):645-647; doi:10.1016/j.cardiores.2004.01.008
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Protease-activated receptors and EDHF: the icing on the cake?

Tobias Traupe and Matthias Barton*

Medizinische Poliklinik, Departement für Innere Medizin, Universitätsspital Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland

* Corresponding author. Tel.: +41-1-255 5663; fax: +41-1-255 8747. barton@usz.ch

Received 29 December 2003; accepted 7 January 2004

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

See article by Kawabata et al. (pages 683–692) in this issue.

The regulation of vascular smooth muscle cell tone by the vascular endothelium was initially described by Furchgott and Zawadzki, suggesting the existence of an endothelium-derived relaxing factor (EDRF) acting through cGMP, which was later identified as nitric oxide (NO) (see reference [1] for review). Since then, other actions of NO such as control of cell growth, blood cell–endothelial cell interactions, immunomodulatory functions, and antiaggregatory effects have been described [2]. In addition to NO and cyclooxygenase products, a third endothelium-derived principle, namely hyperpolarization of vascular smooth muscle cells in response to an endothelium-derived hyperpolarizing factor (EDHF), has been identified described [3]. Production and bioactivity of endothelial factors are disturbed in cardiovascular diseases, and endothelium-dependent dilator mechanisms are counteracted by vasoconstrictory . . . [Full Text of this Article]


   1. Vascular expression and function of protease-activated receptors
 

   2. PAR1 and vascular function: role of the endothelium
 

   3. A link between PAR2 and EDHF?
 

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