Effect of Ca2+ ionophores on membrane potential of pig coronary artery endothelial cells

1992 ◽  
Vol 262 (6) ◽  
pp. H1823-H1831 ◽  
Author(s):  
P. Y. von der Weid ◽  
J. L. Beny
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Maximal Response ◽  
Response Curves ◽  
Direct Role ◽  
Pig Coronary Artery ◽  
Endothelium Dependent Relaxation

Ca2+ ionophores (A23187 and ionomycin) were used to determine whether an increase in cytosolic Ca2+ plays a direct role in pig coronary endothelial cell hyperpolarization. Ionophores induced concentration-dependent hyperpolarizations that were not altered by the presence of N omega-nitro-L-argnine (L-NNA), and inhibitor of nitric oxide synthesis. d-Tubocurarine decreased by 65-89% the A23187- and substance P (SP)-generated hyperpolarization of endothelial cells. To study the role of endothelial cell hyperpolarization in the endothelium-dependent relaxation of precontracted coronary artery strips, A23187 and SP concentration-response curves were built up in the presence of d-tubocurarine and/or L-NNA. A decrease in the maximal response was observed only when both d-tubocurarine and L-NNA were present. Our direct in situ approach gives results in agreement with a gating of Ca(2+)-activated K+ channels during A23187- and SP-induced hyperpolarizations of endothelial cells. We suggest that these hyperpolarizations play a role in the endothelial cell-dependent relaxation induced by A23187 and SP in the pig coronary artery.

Two mechanisms mediate relaxation by bradykinin of pig coronary artery: NO-dependent and -independent responses

1991 ◽  
Vol 261 (3) ◽  
pp. H830-H835 ◽  
Author(s):  
C. L. Cowan ◽  
R. A. Cohen
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Coronary Artery ◽  
Thromboxane A2 ◽  
Porcine Coronary Artery ◽  
Cyclic Monophosphate ◽  
Pig Coronary Artery ◽  
Endothelium Dependent Relaxation

The role of nitric oxide and guanosine 3',5'-cyclic monophosphate (cGMP) accumulation in the endothelium-dependent relaxation of the porcine coronary artery to bradykinin was investigated by comparing relaxation and cGMP accumulation in the presence or absence of NG-monomethyl-L-arginine (L-NMMA) and methylene blue. Rings were treated with indomethacin to eliminate the effects of prostaglandins. Relaxation to bradykinin of rings contracted with the thromboxane A2 mimetic U-46619 was not affected by L-NMMA and was only minimally inhibited by methylene blue. Rings contracted with elevated potassium (25 mM) also relaxed completely to bradykinin. However, L-NMMA or methylene blue effectively inhibited relaxation to bradykinin in rings contracted with potassium. cGMP accumulation was stimulated by bradykinin and inhibited by L-NMMA or methylene blue in rings contracted with either U-46619 or potassium. These results suggest that in the absence of nitric oxide-induced cGMP accumulation, a nonprostanoid mechanism exists that is capable of completely relaxing U-46619-contracted coronary artery. This mechanism is either inhibited in or unable to relax potassium-contracted rings. These results also demonstrate that nitric oxide mediates the bradykinin-induced cGMP accumulation that is largely responsible for the relaxation during contraction with potassium.

scholarly journals Endothelial cell infection in vivo by equine infectious anaemia virus

1999 ◽  
Vol 80 (9) ◽  
pp. 2393-2397 ◽  
Author(s):  
J. Lindsay Oaks ◽  
Catherine Ulibarri ◽  
Timothy B. Crawford
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Infection ◽  
Tissue Macrophage ◽  
Cell Type Specific ◽  
Weakly Virulent ◽  
Equine Infectious Anaemia Virus

Equine infectious anaemia virus (EIAV) infection of horses is characterized clinically by recurrent episodes of fever, thrombocytopenia and anaemia. In vivo, the only site of virus replication that has been previously demonstrated for EIAV is the tissue macrophage. In this study, in situ hybridization for EIAV was combined with immunohistochemistry for cell-type-specific markers to identify infected endothelial cells. EIAV-infected endothelial cells and macrophages were detected in horses infected with either virulent wild-type or with weakly virulent tissue culture-adapted strains of EIAV. The role of endothelial cell infection in the pathogenesis of EIAV remains undefined, but could contribute to the development of thrombocytopenia. However, endothelial cell infection does not appear to be a determinant of virulence for EIAV.

Proapoptotic effects of ANG II in human coronary artery endothelial cells: role of AT1receptor and PKC activation

1999 ◽  
Vol 276 (3) ◽  
pp. H786-H792 ◽  
Author(s):  
Dayuan Li ◽  
Baichun Yang ◽  
M. Ian Philips ◽  
Jawahar L. Mehta
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Specific Inhibitor ◽  
Ang Ii ◽  
Human Coronary Artery ◽  
Tnf Α ◽  
Factor Α ◽  
Pkc Activation

Anoxia-reoxygenation, tumor necrosis factor-α (TNF-α), and angiotensin II (ANG II) have been shown to induce apoptosis in myocytes. However, the role of these mediators in causing apoptosis of human coronary artery endothelial cells (HCAEC) is not known. This study was designed to examine the interaction of these mediators in induction of apoptosis in HCAEC. Cultured HCAEC were exposed to anoxia-reoxygenation, TNF-α, and ANG II. TNF-α enhanced apoptosis of HCAEC (determined by DNA nick-end labeling in situ and DNA laddering) caused by anoxia-reoxygenation. ANG II increased apoptosis beyond that caused by anoxia-reoxygenation and TNF-α. Apoptosis caused by ANG II was reduced by losartan, a specific ANG II type 1 receptor (AT1R) blocker, whereas PD-123,177, a specific ANG II type 2 receptor blocker, under identical conditions had minimal effect. The proapoptotic effects of ANG II were associated with the activation of protein kinase C (PKC). The importance of PKC activation as a signal transduction mechanism became evident in experiments wherein treatment of HCAEC with a specific inhibitor of PKC activation decreased ANG II-mediated apoptosis. Thus AT1R activation appears to be responsible for apoptosis caused by ANG II in HCAEC, and AT1R activation-mediated apoptosis involves activation of PKC.

Abstract 297: Crataegus Special Extract WS 1442 Retards Replicative Senescence in Coronary Artery Endothelial Cells: Role of eNOS-derived NO

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Noureddine Idris-Khodja ◽  
Marouene Kheloufi ◽  
Valérie B Schini-Kerth
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Replicative Senescence ◽  
Critical Role ◽  
Primary Cultures ◽  
Enos Expression ◽  
Potent Inducer ◽  
In Cells

Endothelial cell senescence promotes endothelial dysfunction, which has been suggested to have a critical role in the initiation and/or progression of atherosclerosis, and also to contribute to the pathogenesis of age-associated vascular disorders. Endothelial senescence is characterized by an irreversible cell cycle arrest, which involves an increased activity of p53 and its downstream effector p21. Endothelial senescence is also associated with a decreased expression of endothelial nitric oxide synthase (eNOS). The present study has evaluated whether the Crataegus special extract WS ® 1442, a rich source of polyphenols and a potent inducer of eNOS activation, prevents replicative senescence of porcine coronary artery endothelial cells, and, if so, to elucidate the underlying mechanism. Replicative senescence was induced by sequential passaging of primary cultures of endothelial cells up to the fourth passage (P4). Changes of endothelial senescence were determined by measuring senescence-associated β-galactosidase (SA-β-gal) activity. Western blot was used to analyze the protein expression of p53, p21 and eNOS. Compared to P1, the SA-β-gal activity was 240% increased in cells at P4 ( P <0.001), and this effect was associated with 93% ( P <0.001) and 56% ( P <0.001) increased expression of p53, p21 and a 87% decreased expression of eNOS ( P <0.001). Treatment of P3 cells with the p53 inhibitor (pifithrin) reduced 43% SA-β-gal activity indicating a role of p53 activity in replicative senescence ( P <0.001). Treatment of endothelial cells with the Crataegus extract reduced by 56% the SA-β-gal activity ( P <0.01), improved by 131 % eNOS expression ( P <0.01) and reduced by 39% the up-regulation of p21 in cells at P4 without affecting the expression level of p53. The inhibitor of eNOS, L-NAME promoted the induction of endothelial senescence at P1 and reduced the inhibitory effect of the Crataegus extract on SA-β-gal activity at P3. In conclusion, the present findings indicate that the Crataegus extract delays endothelial cell replicative senescence most likely by preventing the downregulation of eNOS expression and activity and the upregulation of the p53/p21 pathway.

scholarly journals An autoantibody directed against human thrombin anion-binding exosite in a patient with arterial thrombosis: effects on platelets, endothelial cells, and protein C activation

Blood ◽  
1994 ◽  
Vol 84 (6) ◽  
pp. 1843-1850 ◽  
Author(s):  
E Arnaud ◽  
M Lafay ◽  
P Gaussem ◽  
V Picard ◽  
M Jandrot-Perrus ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Arterial Thrombosis ◽  
Protein C ◽  
Receptor Activation ◽  
Anion Binding ◽  
Thrombin Receptor ◽  
Cell Functions ◽  
Human Thrombin

Abstract An autoantibody, developed by a patient with severe and recurrent arterial thrombosis, was characterized to be directed against the anion- binding exosite of thrombin, and inhibited all thrombin interactions requiring this secondary binding site without interfering with the catalytic site. The effect of the antibody was studied on thrombin interactions with platelets and endothelial cells from human umbilical veins (HUVEC). The autoantibody specifically and concentration- dependently inhibited alpha-thrombin-induced platelet activation and prostacyclin (PGI2) synthesis from HUVEC. It had no effect when gamma- thrombin or the thrombin receptor activation peptide SFLLR were the inducers. The effect of the antibody on protein C activation has been studied. The antibody blocked the thrombin-thrombomodulin activation of protein C. The inhibition of the activation was maximal with a low concentration of thrombomodulin. The fact that the autoantibody inhibited concentration-dependent alpha-thrombin-induced platelet and endothelial cell functions emphasizes the crucial role of the anion- binding exosite of thrombin to activate its receptor. In regard to the pathology, the antibody inhibited two vascular processes implicated in thrombin-antithrombotic functions, PGI2 secretion, and protein C activation, which could be implicated in this arterial thrombotic disease.

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.

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