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Cardiovascular Research 2000 46(3):370-375; doi:10.1016/S0008-6363(00)00059-6
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

EDHF and residual NO: different factors

Bert Vanheel* and Johan Van de Voorde

Department of Physiology and Physiopathology, Ghent University, De Pintelaan 185, B-9000 Gent, Belgium

* Corresponding author. Tel.: +32-9-240-3330; fax: +32-9-240-3059 Bert.Vanheel@rug.ac.be

Received 25 February 2000; accepted 25 February 2000

The first 150 words of the full text of this article appear below.

See article by Ge et al. [61] (pages 547–556) in this issue.


   1 Introduction
 
The endothelium plays a pivotal role in the control of vascular tone and blood pressure. In response to a variety of physiological stimuli, such as bradykinin, acetylcholine, histamine, substance P, shear stress and pulsatile stretch, endothelial cells release vasodilator substances. Those include prostacyclin [1] and endothelium-derived relaxing factor (EDRF) [2]. The latter has been identified as nitric oxide (NO) [3]. This labile compound is continuously synthesized from L-arginine by the nitric oxide synthase (NOS) enzyme constitutively expressed in the endothelial cell. It acts by direct stimulation of the soluble guanylyl cyclase in vascular smooth muscle cells. Since the elucidation of the biosynthesis of NO, L-arginine analogues such as NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (L-NA) and its methyl ester (L-NAME) have been used as . . . [Full Text of this Article]


   2 Nitric oxide causes hyperpolarization
 

   3 Residual NO
 

   4 Porcine coronary arteries
 

   5 The study of Ge, Zhang, Fung and He [61]
 

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