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Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor

Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor Endothelium-derived relaxing factor (EDRF) is a labile humoral agent which mediates the action of some vasodilators. Nitrovasodi-lators, which may act by releasing nitric oxide (NO), mimic the effect of EDRF and it has recently been suggested by Furchgott1 that EDRF may be NO. We have examined this suggestion by studying the release of EDRF and NO from endothelial cells in culture. NO was determined as the chemiluminescent product of its reaction with ozone2. The biological activity of EDRF and of NO was measured by bioassay3. The relaxation of the bioassay tissues induced by EDRF was indistinguishable from that induced by NO. Both substances were equally unstable. Bradykinin caused concentration-dependent release of NO from the cells in amounts sufficient to account for the biological activity of EDRF. The relaxations induced by EDRF and NO were inhibited by haemoglobin and enhanced by superoxide dismutase to a similar degree. Thus NO released from endothelial cells is indistinguishable from EDRF in terms of biological activity, stability, and susceptibility to an inhibitor and to a potentiator. We suggest that EDRF and NO are identical. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Springer Journals

Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor

Nature , Volume 327 (6122) – Jun 11, 1987

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Publisher
Springer Journals
Copyright
Copyright © 1987 by Nature Publishing Group
Subject
Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
ISSN
0028-0836
eISSN
1476-4687
DOI
10.1038/327524a0
Publisher site
See Article on Publisher Site

Abstract

Endothelium-derived relaxing factor (EDRF) is a labile humoral agent which mediates the action of some vasodilators. Nitrovasodi-lators, which may act by releasing nitric oxide (NO), mimic the effect of EDRF and it has recently been suggested by Furchgott1 that EDRF may be NO. We have examined this suggestion by studying the release of EDRF and NO from endothelial cells in culture. NO was determined as the chemiluminescent product of its reaction with ozone2. The biological activity of EDRF and of NO was measured by bioassay3. The relaxation of the bioassay tissues induced by EDRF was indistinguishable from that induced by NO. Both substances were equally unstable. Bradykinin caused concentration-dependent release of NO from the cells in amounts sufficient to account for the biological activity of EDRF. The relaxations induced by EDRF and NO were inhibited by haemoglobin and enhanced by superoxide dismutase to a similar degree. Thus NO released from endothelial cells is indistinguishable from EDRF in terms of biological activity, stability, and susceptibility to an inhibitor and to a potentiator. We suggest that EDRF and NO are identical.

Journal

NatureSpringer Journals

Published: Jun 11, 1987

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