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.

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.

Inhibition of endothelium-derived relaxing factor-dependent circulatory control in intact rats

1992 ◽  
Vol 262 (5) ◽  
pp. H1494-H1500 ◽  
Author(s):  
A. L. Loeb ◽  
D. E. Longnecker
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Gastrointestinal Tract ◽  
Vascular Resistance ◽  
Brown Fat ◽  
Mean Blood Pressure ◽  
Relaxing Factor ◽  
Venous Circulation ◽  
Circulatory Control ◽  
Endothelium Derived Relaxing Factor

The effects of the endothelium-derived relaxing factor (EDRF) inhibitors NG-monomethyl-L-arginine (L-NMMA) and methylene blue (MB) on resting hemodynamics and responses to vasodilators were studied in the intact rat anesthetized with pentobarbital sodium. L-NMMA infusions (100 mg/kg) significantly increased mean blood pressure by 48%; this effect was rapidly reversed by L-arginine (300 mg/kg). MB (50 mg/kg) decreased mean blood pressure by 24%. Both MB and L-NMMA significantly attenuated the vasodepressor responses to acetylcholine, ATP, and adenosine. By use of radiolabeled microspheres, it was determined that the blood pressure increase after L-NMMA was due to a marked increase in systemic vascular resistance (SVR; from 1.3 +/- 0.1 to 3.1 +/- 0.3 mmHg.ml-1.min-1) and decreased cardiac output. L-NMMA increased vascular resistance in brain, cerebellum, skin, skeletal muscle, ear, white and brown fat, kidney, spleen, hepatic artery, and gastrointestinal tract. Flow decreased in the skin, kidneys, ear, white and brown fat, gastrointestinal tract, portal venous circulation, and liver in response to L-NMMA. In contrast, MB decreased heart rate, blood pressure, and SVR significantly. MB increased blood flow and decreased vascular resistance in several organs, including the brain, and skeletal muscle. These results indicate that both MB and L-NMMA can inhibit agonist-induced EDRF-mediated vasodepressor responses. However, inhibition of agonist-induced responses did not predict the general and regional hemodynamic responses to L-NMMA or MB infusion.

Endothelium-derived relaxing factor regulates renin release in vivo

1992 ◽  
Vol 263 (2) ◽  
pp. F256-F261 ◽  
Author(s):  
D. H. Sigmon ◽  
O. A. Carretero ◽  
W. H. Beierwaltes
Keyword(s):  
Blood Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renin Release ◽  
Beta Adrenergic ◽  
Synthesis Inhibition ◽  
Renal Perfusion Pressure ◽  
Relaxing Factor ◽  
Endothelium Derived Relaxing Factor

Endothelium-derived relaxing factor (EDRF), through its inhibitory second messenger guanosine 3',5'-cyclic monophosphate (cGMP), inhibits renin release in vitro. To determine whether EDRF affects renin in vivo, we tested whether EDRF synthesis inhibition could stimulate renin secretion in intact rats. Because EDRF synthesis inhibition increases blood pressure and consequently withdraws sympathetic activity (both renin inhibitory signals), we also studied the effect of L-N omega-nitroarginine methyl ester (L-NAME) when renal perfusion pressure was controlled and during beta-adrenergic blockade. Mean blood pressure (BP), heart rate (HR), and plasma renin activity (PRA) were measured in anesthetized rats before and after EDRF synthesis inhibition by a 10 mg/kg body wt bolus of L-NAME. L-NAME decreased PRA by 67% [from 11.0 +/- 2.7 to 3.7 +/- 0.8 ng angiotensin I (ANG I).ml-1.h-1, n = 12; P less than 0.001], increased BP by 20 +/- 2 mmHg (P less than 0.001), and decreased HR from 332 +/- 8 to 312 +/- 9 beats/min (P less than 0.005). We repeated our experiment in rats instrumented with an intra-aortic balloon catheter to control renal perfusion pressure and pretreated with propranolol to eliminate the beta-adrenergic effect. Under these conditions, L-NAME now increased PRA by 55% (from 6.9 +/- 1.9 to 10.8 +/- 2.6 ng ANG I.ml-1.h-1, n = 12; P less than 0.02), whereas renal perfusion pressure was unchanged (91 +/- 4 vs. 90 +/- 4 mmHg). HR increased slightly from 308 +/- 5 to 315 +/- 3 beats/min (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

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