N G-nitro-l-arginine antagonizes endothelium-dependent dilator responses by inhibiting endothelium-derived relaxing factor release in the isolated rabbit heart

1991 ◽  
Vol 418 (3) ◽  
pp. 266-270 ◽  
Author(s):  
Daniel Lamontagne ◽  
Ulrich Pohl ◽  
Rudi Busse
Keyword(s):  
Rabbit Heart ◽  
Relaxing Factor ◽  
Isolated Rabbit Heart ◽  
Endothelium Derived Relaxing Factor ◽  
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.

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.

Anti-EDRF effect of tumor necrosis factor in isolated, perfused cat carotid arteries

1989 ◽  
Vol 256 (5) ◽  
pp. H1509-H1512 ◽  
Author(s):  
N. Aoki ◽  
M. Siegfried ◽  
A. M. Lefer
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Carotid Arteries ◽  
Human Tumor ◽  
Vasodilator Response ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor ◽  
Inhibitor Of Protein Synthesis ◽  
Necrosis Factor ◽  
Factor Release

Cat carotid arteries that have an intact endothelium were isolated and perfused with Krebs-Henseleit solution containing recombinant human tumor necrosis factor (rhTNF). Perfused arteries were preconstricted with KCl and then dilated with acetylcholine (ACh) or acidified NaNO2. After perfusion with TNF (4 micrograms/ml) for 120 min, the ACh-induced vasodilator response was markedly blunted, but the NaNO2 vasodilator response was not significantly affected. Arteries perfused with 2 micrograms/ml TNF for 60-120 min or with 4 micrograms/ml for 60 min did not develop a significantly impaired relaxation to ACh. Moreover, perfusion with 20-100 micrograms/ml cycloheximide, an inhibitor of protein synthesis, blocked the TNF-induced impairment of the relaxation to ACh. On the other hand, the vasodilator response to acidified NaNO2 did not change in any perfused carotid arteries. These results suggest that TNF promotes the synthesis of proteins that contribute to the damage of endothelial cells directly, probably by inhibiting endothelium-derived relaxing factor release.

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