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Cardiovascular Research 2007 75(2):207-209; doi:10.1016/j.cardiores.2007.05.023
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Copyright © 2007, European Society of Cardiology

Nitric oxide signaling comes of age: 20 years and thriving

Santiago Lamasa,*, Charles J. Lowensteinb and Thomas Michelc

aCentro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas and Instituto "Reina Sofía" de Investigaciones Nefrológicas, Ramiro de Maeztu, 9, Madrid E-28040, Spain
bThe Johns Hopkins University School of Medicine, 950 Ross Bldg., 720 Rutland Ave., Baltimore, MD 21205, USA
cDepartment of Medicine, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA

* Corresponding author. Centro de Investigaciones Biológicas-CSIC, Ramiro de Maeztu 9, Madrid, 28040, Spain. Tel.: +34 91 837 3112x4302, +34 64 941 8799 (mobile); fax: +34 91 536 0432. slamas@cib.csic.es

Received 25 May 2007; accepted 30 May 2007

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

The lyrics of a famous tango state that "twenty years time is just nothing". While this impression may broadly apply to different circumstances, such might not be the case for nitric oxide (NO). In the year 1987 two seminal contributions coming from independent laboratories [1,2] established the identity of the elusive endothelial derived relaxing factor reported by Bob Furchgott seven years earlier [3]. These laboratories showed that the chemical nature of "endothelium-derived relaxing factor" (EDRF) was identical to NO. The idea that NO could act as an activator of soluble guanylate cyclase had been proposed even earlier [4]. These four papers, together with the demonstration of L-arginine as substrate for the generation of NO [5], defined a pathway in endothelial cells which is now considered classical: the L-arginine-NO-cGMP pathway. Of importance, a considerable amount of information had already accumulated almost at the same time and . . . [Full Text of this Article]


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