Endothelium-derived relaxing factor release on activation of NMDA receptors suggests role as intercellular messenger in the brain

Nature ◽  
1988 ◽  
Vol 336 (6197) ◽  
pp. 385-388 ◽  
Author(s):  
John Garthwaite ◽  
Sarah L. Charles ◽  
Russell Chess-Williams
Keyword(s):  
Nmda Receptors ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
The Brain ◽  
Intercellular Messenger ◽  
Factor Release

Endothelium derived relaxing factor release from canine coronary artery by leukocytes

1995 ◽  
Vol 73 (3) ◽  
pp. 404-408 ◽  
Author(s):  
Joseph F. Kleha ◽  
Pierre Devesly ◽  
Anthony Johns
Keyword(s):  
Endothelial Cell ◽  
Coronary Artery ◽  
Human Monocyte ◽  
Relaxing Factor ◽  
Canine Coronary Artery ◽  
Endothelium Derived Relaxing Factor ◽  
Ly 83583 ◽  
Muscle Calcium ◽  
Endothelium Dependent Relaxation ◽  
Factor Release

Lectins, known to recognize endothelial cell adhesion molecules, have been shown to release endothelium-derived relaxing factor (EDRF) from blood vessels. We investigated the effects of different leukocyte-type cells to determine if these cells, by interacting with the endothelium, could release EDRF from the circumflex branch of the canine coronary artery. The following cells were investigated: human promyelocytic leukemia (HL-60), human monocyte (THP-1), and human Burkitt lymphoma (DAUDI). All of these cells produced a significant endothelium-dependent relaxation of the dog coronary artery in the presence of ibuprofen. The endothelium-dependent relaxations were reversed by hemoglobin (10 μM), methylene blue (3 μM), 6-anilino-5,8-quinolinedione (LY 83583, 30 μM), and NG-nitro-L-arginine methyl ester (L-NAME, 1 mM). HL-60 cells grown in the presence of 1 mM L-NAME retained their ability to cause endothelium-dependent relaxation of the canine coronary artery, suggesting that the source of the NO was the endothelium and not the HL-60 cells. The cell-induced vascular relaxation could be obtained in the absence of extracellular calcium. It is suggested that HL-60, THP-1, and DAUDI cells interact with a specific receptor on the endothelial cell and as a result of this interaction the endothelial cells are stimulated to release EDRF.Key words: endothelium-derived relaxing factor, nitric oxide, endothelium, HL-60, DAUDI, THP-1, smooth muscle, calcium, contraction, canine coronary artery.

Inducible NO synthase: role in cellular signalling

1999 ◽  
Vol 202 (6) ◽  
pp. 645-653 ◽  
Author(s):  
K.F. Beck ◽  
W. Eberhardt ◽  
S. Frank ◽  
A. Huwiler ◽  
U.K. Messmer ◽  
...  
Keyword(s):  
Gene Expression ◽  
No Synthase ◽  
Signalling Pathways ◽  
Target Cells ◽  
Activated Macrophages ◽  
The Past ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Intercellular Messenger

The discovery of endothelium-derived relaxing factor and its identification as nitric oxide (NO) was one of the most exciting discoveries of biomedical research in the 1980s. Besides its potent vasodilatory effects, NO was found under certain circumstances to be responsible for the killing of microorganisms and tumour cells by activated macrophages and to act as a novel, unconventional type of neurotransmitter. In 1992, Science picked NO as the ‘Molecule of the Year’, and over the past years NO has become established as a universal intercellular messenger that acutely affects important signalling pathways and, on a more long-term scale, modulates gene expression in target cells. These actions will form the focus of the present review.

Role of endothelium-derived relaxing factor in cerebral circulation: large arteries vs. microcirculation

1991 ◽  
Vol 261 (4) ◽  
pp. H1038-H1042 ◽  
Author(s):  
F. M. Faraci
Keyword(s):  
Cerebral Circulation ◽  
Vessel Diameter ◽  
Cerebral Blood Vessels ◽  
Large Arteries ◽  
Small Vessels ◽  
Relaxing Factor ◽  
Basal Tone ◽  
Endothelium Derived Relaxing Factor ◽  
The Brain

This study examined the hypothesis that formation of endothelium-derived relaxing factor (EDRF) in the brain has a greater influence on basal tone in large arteries than arterioles. Diameters of the basilar artery and its branches and of arterioles on the cerebrum were measured through cranial windows in anesthetized rats. Under control conditions, topical application of NG-monomethyl-L-arginine (L-NMMA), which inhibits formation of EDRF or nitric oxide (NO) from L-arginine, produced concentration-related constriction that was dependent on initial vessel diameter. Large arteries [diameter = 275 +/- 10 microns (mean +/- SE)] constricted by 10.4 +/- 0.8% in response to 10(-5) M L-NMMA. In contrast, arterioles (62 +/- 6 microns) constricted by only 3.7 +/- 0.6% (P less than 0.01 vs. large arteries), regardless of brain region. U-46619 produced similar constriction of large arteries and arterioles, which indicates that reduced responses to L-NMMA in arterioles is not due to impaired constrictor capacity. Sodium nitroprusside produced similar dilatation of large arteries and arterioles, which suggests that activity of guanylate cyclase is not reduced in small vessels. Dilator responses of large arteries and arterioles to acetylcholine, but not nitroprusside, were inhibited by L-NMMA. Thus synthesis of EDRF from L-arginine influences basal tone of cerebral blood vessels, and the effect is greatest in large arteries. In contrast, the role of EDRF or NO in mediating responses to acetylcholine in the cerebral circulation is similar in large arteries and the microcirculation.

Increases in NO2−/NO3− excretion in the urine as an indicator of the release of endothelium-derived relaxing factor during elevation of blood pressure

1992 ◽  
Vol 82 (6) ◽  
pp. 631-634 ◽  
Author(s):  
Hiromichi SUZUKI ◽  
Hideki IKENAGA ◽  
Keiichi HISHIKAWA ◽  
Toshio NAKAKI ◽  
Ryuichi KATO ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Urinary Excretion ◽  
Renal Denervation ◽  
Sudden Increase ◽  
Mechanical Pressure ◽  
Kidney Weight ◽  
Relaxing Factor ◽  
Neural Factors ◽  
Endothelium Derived Relaxing Factor ◽  
Factor Release

1. Under hormonally constant conditions, the effects of a sudden increase in blood pressure on the release of endothelium-derived relaxing factor were evaluated by measuring urinary excretion of NO2−/NO3− in rats with renal denervation. 2. Elevation of blood pressure from 136 ± 2 to 153 ± 3 mmHg by an aortic clamp below the renal arteries induced a significant increase in urinary excretion of NO2−/NO3− from 76.6 ± 4.2 × 102 to 108.1 ± 8.3 × 102 pmol min−1 g−1 kidney weight (P < 0.05). 3. Infusion of NG−monomethyl-L-arginine (1 mg min−1 kg−1) without an aortic clamp raised mean blood pressure to a similar level; however, urinary excretion of NO2−/ NO3− was decreased significantly. 4. During infusion of NG−monomethyl-L-arginine, aortic occlusion caused a significant increase in blood pressure without any changes in NO2−/NO3− excretion in the urine. 5. These results suggest that the formation of NO, an indicator of endothelium-derived relaxing factor release, was increased by mechanical pressure elevation without apparent changes in hormonal and neural factors.

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