Copyright © 2007, European Society of Cardiology
NO with no NOS in ischemic heart
Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry New Jersey, New Jersey Medical School, 185 South Orange Avenue, MSB G-609, Newark, NJ, United States
* Corresponding author. Tel.: +1 973 972 3926; fax: +1 973 972 7489. Email address: deprech@umdnj.edu
Received 2 February 2007; accepted 6 February 2007
| The first 10% of the full text of this article appears below. |
See article by Martin et al. [5] (pages 46–55) in this issue.
The seminal observation by Furchgott and Zawadzki [1] of a paradoxical vasoconstrictive effect of acetylcholine in arteries deprived of endothelium paved the way for the rapid discovery of nitric oxide (NO) and of the mechanisms of NO generation by a specific family of isoforms known as NO synthases (NOS). The role of NO in the endothelium was characterized as a predominant mechanism of vasodilation through the production of cyclic GMP (cGMP) in vascular smooth muscle cells. The rapid progress of this research in endothelial cells automatically led to the question whether the cardiac cell itself could be a source of NO.
It was found that the three characterized isoforms of NOS are expressed in cardiac myocytes [2]