Endothelin B Receptor Antagonist Increases Preproendothelin-1 Transcription in Bovine Aortic Endothelial Cells and In Vivo

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.2.h630 ◽

2000 ◽

Vol 279 (2) ◽

pp. H630-H638 ◽

Cited By ~ 21

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.

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Influence of Nicotine and Cotinine on the Expression of Plasminogen Activator Activity in Bovine Aortic Endothelial Cells

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646529 ◽

1989 ◽

Vol 61 (01) ◽

pp. 070-076 ◽

Cited By ~ 11

Author(s):

Be-Sheng Kuo ◽

Maciej Dryjski ◽

Thorir D Bjornsson

Keyword(s):

Endothelial Cells ◽

Plasminogen Activator ◽

Plasminogen Activator Inhibitor ◽

Dependent Manner ◽

Aortic Endothelial Cells ◽

Bovine Aortic Endothelial Cells ◽

Fibrin Plate ◽

Sds Page ◽

Aortic Endothelial

SummaryThe effects of nicotine and its major metabolite, cotinine, were evaluated on the secretion of plasminogen activator (PA) and plasminogen activator inhibitor (PAI) in cultured bovine aortic endothelial cells. Both compounds increased PA secretion, determined by 125I-fibrin plate assay, in a time- and dose-dependent manner. Maximum effects after 24 hr incubation were observed for nicotine at 10-8 M and for cotinine at 10-7 M, which corresponded to about 2.6-fold increases over control for both compounds. The pharmacological PA stimulation required both RNA and protein syntheses, as evidenced by inhibition by acfinomycin D and cycloheximide. Both control and treated cells produced multiple forms of PA, as evaluated by SDS-PAGE zymography, and a single form of PAI, as evidenced by reverse fibrin autography. Although activities of all species of PA were enhanced by nicotine and cotinine, these compounds had no significant effects on the release of PAI. These results thus suggest that nicotine and cotinine may have fibrinolytic activity in vivo.

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

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657338 ◽

1983 ◽

Vol 49 (02) ◽

pp. 132-137 ◽

Cited By ~ 16

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.

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