Endothelium-derived relaxant factor inhibits effects of nitrocompounds in isolated arteries

1987 ◽  
Vol 252 (2) ◽  
pp. H307-H313
Author(s):  
U. Pohl ◽  
R. Busse
Keyword(s):  
Endothelial Cells ◽  
Femoral Artery ◽  
Response Curve ◽  
Rabbit Aorta ◽  
Nordihydroguaiaretic Acid ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Basal Release ◽  
Isolated Arteries

We investigated the influence of endothelial cells on the smooth muscle vasodilator effects to sodium nitroprusside (SNP) or Teopranitol (an organic mononitrate) in isolated segments of rabbit aorta and femoral artery. In the femoral artery, the vasodilator responses to both nitrocompounds were significantly higher in the absence of endothelial cells or after pretreatment with the endothelium-derived relaxant factor (EDRF) inhibitor nordihydroguaiaretic acid (NDGA; 10 microM). Moreover, under conditions of stimulated EDRF release (induced by acetylcholine; 30–100 nM) the vasodilator responses to SNP were further attenuated in vessels with intact endothelium. By contrast, in the rabbit aorta, the vasodilator responses to the nitrocompounds were not significantly altered by either endothelium removal or treatment with NDGA. However, in the presence of the EDRF stimulator acetylcholine, the dose-response curve to SNP was shifted to right in the aorta as well. The role of EDRF in the endothelium-mediated attenuation of the dilator potency of SNP was further investigated by using EDRF released from cultured (bovine aortic) endothelial cells. The dilator effects of SNP were compared in endothelium denuded femoral or aortic segments in the presence or absence of EDRF. The vasodilator effects of SNP in both types of arteries were significantly reduced in the presence of EDRF. We conclude that EDRF attenuates the arterial vasodilation induced by SNP and Teopranitol. The results further suggest that endothelial cells exhibit a greater basal release of EDRF in the femoral artery than in the aorta, since under unstimulated conditions an EDRF-induced attenuation was seen only in femoral and not in aortic segments.

Adenoviral expression of 15-lipoxygenase-1 in rabbit aortic endothelium: role in arachidonic acid-induced relaxation

2007 ◽  
Vol 292 (2) ◽  
pp. H1033-H1041 ◽  
Author(s):  
Nitin T. Aggarwal ◽  
Blythe B. Holmes ◽  
Lijie Cui ◽  
Helena Viita ◽  
Seppo Yla-Herttuala ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Rabbit Aorta ◽  
Epoxyeicosatrienoic Acid ◽  
Aortic Endothelial Cells ◽  
Aortic Endothelium ◽  
Rate Limiting Step ◽  
Immunohistochemical Studies ◽  
Rate Limiting

Endothelium-dependent vasorelaxation of the rabbit aorta is mediated by either nitric oxide (NO) or arachidonic acid (AA) metabolites from cyclooxygenase (COX) and 15-lipoxygenase (15-LO) pathways. 15-LO-1 metabolites of AA, 11,12,15-trihydroxyeicosatrienoic acid (THETA), and 15-hydroxy-11,12-epoxyeicosatrienoic acid (HEETA) cause concentration-dependent relaxation. We tested the hypothesis that in the 15-LO pathway of AA metabolism, 15-LO-1 is sufficient and is the rate-limiting step in inducing relaxations in rabbit aorta. Aorta and rabbit aortic endothelial cells were treated with adenoviruses containing human 15-LO-1 cDNA (Ad-15-LO-1) or β-galactosidase (Ad-β-Gal). Ad-15-LO-1-transduction increased the expression of a 75-kDa protein corresponding to 15-LO-1, detected by immunoblotting with an anti-human15-LO-1 antibody, and increased the production of HEETA and THETA from [14C]AA. Immunohistochemical studies on Ad-15-LO-1-transduced rabbit aorta showed the presence of 15-LO-1 in endothelial cells. Ad-15-LO-1-treated aortic rings showed enhanced relaxation to AA (max 31.7 ± 3.2%) compared with Ad-β-Gal-treated (max 12.7 ± 3.2%) or control nontreated rings (max 13.1 ± 1.6%) ( P < 0.01). The relaxations in Ad-15-LO-1-treated aorta were blocked by the 15-LO inhibitor cinnamyl-3,4-dihydroxy-a-cyanocinnamate. Overexpression of 15-LO-1 in the rabbit aortic endothelium is sufficient to increase the production of the vasodilatory HEETA and THETA and enhance the relaxations to AA. This confirms the role of HEETA and THETA as endothelium-derived relaxing factors.

Hypoxia stimulates release of endothelium-derived relaxant factor

1989 ◽  
Vol 256 (6) ◽  
pp. H1595-H1600 ◽  
Author(s):  
U. Pohl ◽  
R. Busse
Keyword(s):  
Endothelial Cells ◽  
Femoral Artery ◽  
Aortic Endothelial Cells ◽  
Small Arteries ◽  
Continuous Release ◽  
Bovine Aortic Endothelial Cells ◽  
Partial Pressures ◽  
Intact Rabbit ◽  
Aortic Endothelial

It was tested whether hypoxia stimulates the release of endothelium-derived relaxant factor (EDRF). In paired segments (with and without endothelium) of either femoral artery (n = 49) or aorta (n = 42) from rabbits, selective luminal hypoxia (Po2 = 24 +/- 8 mmHg) was induced, whereas the Po2 at the adventitial side was kept above 300 mmHg. Hypoxia induced a dilation of 11 +/- 2% in aortic segments with endothelium, whereas the paired segments without endothelium dilated by only 1.2 +/- 0.2% (P less than 0.001). Similar results were obtained in femoral segments (11.8 +/- 1.5% dilation in segments with endothelium vs. 1.4 +/- 0.2% in segments without; P less than 0.001). Likewise in 19 out of 36 bioassay experiments, perfusate from endothelium-intact rabbit aortas or cultured bovine aortic endothelial cells exposed to hypoxia elicited dilation (10.7 +/- 3.2%) in the detector. The EDRF-inhibitors, hemoglobin (5 microM) and dithiothreitol (200 microM), significantly inhibited the hypoxia-induced dilation of intact segments as well as of assay segments perfused with effluent from hypoxic donors. These results suggest that hypoxia stimulates the release of EDRF from native and cultured endothelium. Low partial pressures of oxygen, such as those that exist in small arteries and arterioles, might therefore be a physiological stimulus for continuous release of EDRF.

Role of Flavoproteins in Mediating Cellular Responses to 15-deoxy-Δ12,14-prostaglandin J2 in Bovine Aortic Endothelial Cells

2010 ◽  
Vol 49 ◽  
pp. S137
Author(s):  
Stephanie Brook Wall ◽  
Karina C. Ricart ◽  
Fen Zhou ◽  
Michelle S. Johnson ◽  
Praveen Vayalil Kumar ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cellular Responses ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Prostaglandin J2 ◽  
Aortic Endothelial

scholarly journals Ehrlichia ruminantium uses its transmembrane protein Ape to adhere to host bovine aortic endothelial cells

2021 ◽  
Author(s):  
Valerie Pinarello ◽  
Elena Bencurova ◽  
Isabel Marcelino ◽  
Olivier Gros ◽  
Carinne Puech ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Host Cell ◽  
Transmembrane Protein ◽  
Host Cells ◽  
Ehrlichia Ruminantium ◽  
Aortic Endothelial Cells ◽  
Bovine Aortic Endothelial Cells ◽  
Early Interaction ◽  
Aortic Endothelial

Ehrlichia ruminantium is an obligate intracellular bacterium, transmitted by ticks of the genus Amblyomma and responsible for heartwater, a disease of domestic and wild ruminants. High genetic diversity of E. ruminantium strains hampers the development of an effective vaccine against all strains present in the field. In order to develop strategies for the control of heartwater through both vaccine and alternative therapeutic approaches, it is important to first gain a better understanding of the early interaction of E. ruminantium and its host cell. Particularly, the mechanisms associated with bacterial adhesion remain to elucidate. Herein, we studied the role of E. ruminantium membrane protein ERGA_CDS_01230 (UniProt Q5FFA9), a probable iron transporter, in the adhesion process to host bovine aortic endothelial cells (BAEC). The recombinant version of the protein ERGA_CDS_01230, successfully produced in the Leishmania tarentolae system, is O-glycosylated. Following in vitro culture of E. ruminantium in BAEC, the expression of CDS ERGA_CDS_01230 peaks at the extracellular infectious elementary body stages. This result suggest the likely involvement of ERGA_CDS_01230, named hereafter Ape for Adhesion protein of Ehrlichia, in the early interaction of E. ruminantium with its host cells. We showed using flow cytometry and scanning electron microscopy that beads coated with recombinant ERGA_CDS_01230 (rApe) adheres to BAEC. In addition, we also abserved that rApe interacts with proteins of the cell lysate, membrane and organelle fractions. Additionally, enzymatic treatment degrading dermatan and chondroitin sulfates on the surface of BAEC is associated with a 50% reduction in the number of bacteria in the host cell after a development cycle, indicating that glycosaminoglycans seem to play a role in the adhesion of E. ruminantium to the host cell. Finally, Ape induces a humoral response in vaccinated animals. Globally, our work identifying the role of Ape in E. ruminantium adhesion to host cells makes it a gold vaccine candidate and represents a first step toward the understanding of the mechanisms of cell invasion by E. ruminantium.

Permeability of endothelial monolayers to albumin is increased by bradykinin and inhibited by prostaglandins

2001 ◽  
Vol 280 (4) ◽  
pp. L732-L738 ◽  
Author(s):  
Pierre J. Farmer ◽  
Sylvie G. Bernier ◽  
Andrée Lepage ◽  
Gaétan Guillemette ◽  
Domenico Regoli ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adenylate Cyclase ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Intracellular Level ◽  
Concentration Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Endothelial Monolayers ◽  
Bovine Aortic Endothelial Cells

Using monolayers of bovine aortic endothelial cells (BAEC) in modified Boyden chambers, we examined the role of prostaglandins (PGs) in the bradykinin (BK)-induced increase of albumin permeability. BK induced a concentration-dependent increase of the permeability of BAEC, which reached 49.9 ± 1% at the concentration of 10−8 M. Two inhibitors of the prostaglandin G/H synthase, indomethacin (2.88 μM) and ibuprofen (10 μM), potentiated BK-induced permeability 1.8- and 3.9-fold, respectively. Exogenously administered PGE2and iloprost, a stable analog of prostacyclin, attenuated the effect of BK in a concentration-dependent manner. Butaprost equally reduced the effect of BK, suggesting the participation of the EP2receptor in this phenomenon. However, the EP4-selective antagonist AH-23848 did not significantly inhibit the protective effect of PGE2. The inhibitory effect of PGE2 was reversed by the adenylate cyclase inhibitor MDL-12330A (10 μM). These results suggest that BK-induced increase of permeability of BAEC monolayer to 125I-labeled albumin is negatively regulated by PGs. This postulated autocrine activity of PGs may involve an increase in the intracellular level of cAMP.

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.

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