Effects of Dipyrone on Prostaglandin Production by Human Platelets and Cultured Bovine Aortic Endothelial Cells

1983 ◽  
Vol 49 (02) ◽  
pp. 132-137 ◽  
Author(s):  
A Eldor ◽  
G Polliack ◽  
I Vlodavsky ◽  
M Levy
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Competitive Inhibition ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Ionophore A23187 ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

SummaryDipyrone and its metabolites 4-methylaminoantipyrine, 4-aminoantipyrine, 4-acetylaminoantipyrine and 4-formylaminoan- tipyrine inhibited the formation of thromboxane A2 (TXA2) during in vitro platelet aggregation induced by ADP, epinephrine, collagen, ionophore A23187 and arachidonic acid. Inhibition occurred after a short incubation (30–40 sec) and depended on the concentration of the drug or its metabolites and the aggregating agents. The minimal inhibitory concentration of dipyrone needed to completely block aggregation varied between individual donors, and related directly to the inherent capacity of their platelets to synthesize TXA2.Incubation of dipyrone with cultured bovine aortic endothelial cells resulted in a time and dose dependent inhibition of the release of prostacyclin (PGI2) into the culture medium. However, inhibition was abolished when the drug was removed from the culture, or when the cells were stimulated to produce PGI2 with either arachidonic acid or ionophore A23187.These results indicate that dipyrone exerts its inhibitory effect on prostaglandins synthesis by platelets or endothelial cells through a competitive inhibition of the cyclooxygenase system.

scholarly journals Urea transporters are distributed in endothelial cells and mediate inhibition of l-arginine transport

2002 ◽  
Vol 283 (3) ◽  
pp. F578-F582 ◽  
Author(s):  
Laszlo Wagner ◽  
Janet D. Klein ◽  
Jeff M. Sands ◽  
Chris Baylis
Keyword(s):  
Endothelial Cells ◽  
Cell Types ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Wide Distribution ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Elevated Blood Urea Nitrogen ◽  
Aortic Endothelial

Our laboratory previously reported that uremic levels of urea inhibitl-arginine (l-Arg) transport into endothelial cells. The present study further investigated this effect. We measuredl-Arg transport in cultured bovine aortic endothelial cells with normal or high urea (25 mM). The urea transport inhibitor phloretin abolished the inhibitory effect of urea on l-Arg transport, suggesting a role for urea transporters (UTs). We screened bovine aortic endothelial cells and several other endothelial cell types for the presence of UTs by using Western blot analysis. UT-B was present in all endothelial cells, irrespective of species or location of derivation, whereas UT-A distribution was variable and sparse. UT-B was also abundant in rat aorta, mesenteric blood vessels, and spinotrapezius muscle, whereas UT-A distribution was, again, variable and sparse. Chronic elevation of urea had variable, inconsistent effects on UT abundance. This study showed that urea must enter endothelial cells, probably by UT-B, to inhibit l-Arg transport. In view of the wide distribution of UT-B in rat vasculature, elevated blood urea nitrogen may lead to endothelial l-Arg deficiency in vivo.

Hypotonic stress-induced dual Ca2+ responses in bovine aortic endothelial cells

2000 ◽  
Vol 279 (2) ◽  
pp. H630-H638 ◽  
Author(s):  
Masahiro Oike ◽  
Chiwaka Kimura ◽  
Tetsuya Koyama ◽  
Miyuki Yoshikawa ◽  
Yushi Ito
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Receptor Antagonist ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Luciferase Assay ◽  
Aortic Endothelial Cells ◽  
Hypotonic Stress ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

We have investigated the effects of hypotonic stress on intracellular calcium concentration ([Ca2+]i) in bovine aortic endothelial cells. Reducing extracellular osmolarity by 5% to 40% elicited a steep Ca2+ transient both in normal Krebs and Ca2+-free solutions. The hypotonic stress-induced Ca2+ transient was inhibited by phospholipase C inhibitors (neomycin and U-73122), a P2-receptor antagonist (suramin), and an ATP-hydrolyzing enzyme (apyrase), suggesting that the hypotonic stress-induced Ca2+ transient is mediated by ATP. A luciferin-luciferase assay confirmed that 40% hypotonic stress released 91.0 amol/cell of ATP in 10 min. When the hypotonic stress-induced fast Ca2+ transient was inhibited by neomycin, suramin, or apyrase, a gradual [Ca2+]i increase was observed instead. This hypotonic stress-induced gradual [Ca2+]iincrease was inhibited by a phospholipase A2 inhibitor, 4-bromophenacyl bromide. Furthermore, exogenously applied arachidonic acid induced a gradual [Ca2+]i increase with an ED50 of 13.3 μM. These observations indicate that hypotonic stress induces a dual Ca2+ response in bovine aortic endothelial cells, i.e., an ATP-mediated fast Ca2+transient and an arachidonic acid-mediated gradual Ca2+increase, the former being the predominant response in normal conditions.

Large Negative Stress Phase Angle (SPA) Attenuates Nitric Oxide Production in Bovine Aortic Endothelial Cells

2006 ◽  
Vol 128 (3) ◽  
pp. 329-334 ◽  
Author(s):  
Michael B. Dancu ◽  
John M. Tarbell
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Phase Angle ◽  
Aortic Endothelial Cells ◽  
Temporal Phase ◽  
Bovine Aortic Endothelial Cells ◽  
Stress Phase Angle ◽  
Aortic Endothelial

Hemodynamics plays an important role in cardiovascular physiology and pathology. Pulsatile flow (Q), pressure (P), and diameter (D) waveforms exert wall shear stress (WSS), normal stress, and circumferential strain (CS) on blood vessels. Most in vitro studies to date have focused on either WSS or CS but not their interaction. Recently, we have shown that concomitant WSS and CS affect EC biochemical response modulated by the temporal phase angle between WSS and CS (stress phase angle, SPA). Large negative SPA has been shown to occur in regions of the circulation where atherosclerosis and intimal hyperplasia are prevalent. Here, we report that nitric oxide (NO) biochemical secretion was significantly decreased in response to a large negative SPA of −180 deg with respect to an SPA of 0° in bovine aortic endothelial cells (BAEC) at 5 h. A new hemodynamic simulator for the study of the physiologic SPA was used to provide the hemodynamic conditions of pro-atherogenic (SPA=−180 deg) and normopathic (SPA=0 deg) states. The role of complex hemodynamics in vascular remodeling, homeostasis, and pathogenesis can be advanced by further assessment of the hypothesis that a large negative SPA is pro-atherogenic.

scholarly journals Stimulation of In Vitro Angiogenesis by Tetrahydrobiopterin in Bovine Aortic Endothelial Cells

1999 ◽  
Vol 80 (2) ◽  
pp. 177-180 ◽  
Author(s):  
Shunichi Shimizu ◽  
Masako Yasuda ◽  
Masakazu Ishii ◽  
Tsutomu Nagai ◽  
Yuji Kiuchi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
In Vitro Angiogenesis ◽  
Stimulation Of ◽  
Aortic Endothelial

Vitamin E Binds to Specific Binding Sites and Enhances Prostacyclin Production by Cultured Aortic Endothelial Cells

1992 ◽  
Vol 68 (06) ◽  
pp. 744-751 ◽  
Author(s):  
Makoto Kunisaki ◽  
Fumio Umeda ◽  
Toyoshi Inoguchi ◽  
Hajime Nawata
Keyword(s):  
Endothelial Cells ◽  
Vitamin E ◽  
Binding Sites ◽  
Specific Binding ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Specific Binding Sites ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

SummaryWe evaluated the effect of d-α-tocopherol (vitamin E) on the production of prostacyclin (PGI2) by cultured bovine aortic endothelial cells. Vitamin E at physiological doses significantly enhanced the production of PGI2 by aortic endothelial cells when added to the culture simultaneously with histamine, the Ca2+ ionophore A23187 (A23187), plasma-derived serum (PDS), or arachidonic acid. This effect was found to occur in a time- and dose-dependent manner, and the maximal enhancement was produced by 9.28 µM of vitamin E for 1 h incubations. Significantly lower amounts of lipid peroxides were measured in endothelial cells stimulated by 10% PDS with 9.28 µM of vitamin E than in those stimulated without vitamin E for over 24 h, although the stimulation during the initial 1 to 12 h period did not have a significant effect on lipid peroxide formation in cultured aortic endothelial cells.We also demonstrated that bovine aortic endothelial cells have specific binding sites for [3H]vitamin E that exhibited time- and temperature-dependent saturability. At 4° C, the nonspecific binding was 8–12% of the total binding, and the specific binding reached equilibrium by 2 h. Specific binding increased with the concentration of [3H]vitamin E and became saturated at concentrations between 1.5 µM and 2.0 µM per 2.0 × 105 cells. Raising the unlabeled vitamin E concentration from 97.7 nM to 1,000 µM reduced the specific binding of 2.0 µM [3H]vitamin E. The Scatchard plot of [3H]vitamin E binding to the endothelial cells shows two classes of binding sites: one with a high affinity {K a1 2.48 ± 0.32 × 107 NT-1, n = 6} and a low capacity {n 1 1.20 ± 0.34 × 107 sites/cell} and the other with a low affinity {K a2 1.18 ± 0.32 × 105 M–1} and a high capacity {n 2 3.39 ± 0.53 × 109 sites/cell}.Our results suggest that the endothelial cells binding sites for vitamin E may play some roles in vascular homeostasis in vivo, and that vitamin E may prevent the development of atherosclerotic changes due in part to the enhancement of PGI2 production by the vascular wall and its action as an antioxidant in vascular endothelial cell.

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