Wyniki wyszukiwania

1

Control of the circulation by chemical mediators from the endothelium

100%

Vane J. R., Botting R. M.

Journal of Physiology and Pharmacology. Supplement

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1993

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tom 44

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nr 2

2

Cyclooxygenase pathways

86%

Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.

Acta Biochimica Polonica

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2014

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tom 61

|

nr 4

3

Prenatal exposure to hyperoxia modifies the thromboxane prostanoid receptor-mediated response to H2O2 in the ductus arteriosus of the chicken embryo

86%

van der Sterren S., Kessels L., Perez-Vizcaino F., Cogolludo A. L., Villamor E.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 2

4

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Labile products of vascular endothelium as mediators and modulators of the functions of the central nervous system

86%

Dembinska-Kiec A., Goscinski I., Szczudlik A.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 2

5

Actions and interactions of endothelins, prostacyclin and nitric oxide in the gastric mucosa

86%

Whittle B. J. R., Lopez-Belmonte J.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 2

6

The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

72%

Pecanha F. M., Wiggers G. A., Briones A. M., Perez-Giron J. V., Miguel M., Garcia-Redondo A. B., Vassallo D. V., Alonso M. J., Salaices M.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 1

29-36

We have previously demonstrated that chronic exposure to low-dose of mercury induced endothelial dysfunction and increased vasoconstrictor responses. The aim of this work was to investigate if mercury exposure alters contractile prostanoids production from cyclooxygenase-2 (COX-2) and its contribution to phenylephrine responses. For this, aortic segments from 3-month old Wistar rats daily treated with HgCl2 (1st dose 4.6 µg/kg, subsequent dose 0.07 µg/kg/day, i.m.) or vehicle for 30 days were used. Mercury treatment did not affect systolic blood pressure but increased phenylephrine-induced vasoconstriction. The non selective COX inhibitor, indomethacin (10 µmol/l) reduced the response to phenylephrine more in aortic segments from mercury-treated than control rats. The selective COX-2 inhibitor NS 398 (1 µmol/l), the thromboxane A2/prostaglandin H2 receptor (TP) antagonist SQ 29,548 (1 µmol/l), the TXA2 synthase inhibitor furegrelate (1 µmol/l), the EP1 receptor antagonist SC 19220 (1 µmol/l) and the AT1 receptor antagonist losartan (10 µmol/l) reduced phenylephrine response only in vessels from mercury-treated rats. TXA2 and PGE2 levels were greater in the incubation medium of vessels from treated than untreated rats; NS 398 decreased these levels only in the mercury group. COX-2 protein was localized in adventitial and endothelial cells. Aortic COX-2 mRNA expression and plasma angiotensin converting enzyme activity were greater in mercury-treated rats. These results suggest that treatment with low doses of mercury increases the release of COX-2-derived vasoconstrictor prostanoids and its participation in phenylephrine responses. The increased activation of the renin-angiotensin system after mercury treatment might be associated to this increased COX-2 activity.

7

Losartan inhibits the adhesion of rat platelets to fibrillar collagen - a potential role of nitric oxide and prostanoids

72%

Matys T., Chabielska E., Pawlak R., Kucharewicz I., Buczko W.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 4,1

8

The effect of reactive oxygen species on the synthesis of prostanoids from arachidonic acid

58%

Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 4

9

Regulation of the expression of cyclooxygenases and production of prostaglandin I2 and E2 in human coronary artery endothelial cells by curcumin

58%

Tan X., Poulose E. M., Raveendran V. V., Zhu B.-T., Stechschulte D. J., Dileepan K. N.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 1

Curcumin regulates prostaglandin (PG) synthesis in a variety of cells. PGE2 and PGI2 are generated from arachidonic acid (AA) by cyclooxygenases 1 and 2 (COX-1 and COX-2) and the synthase (PGES and PGI2S) pathways. This study evaluates the in vitro effect of curcumin on the expression of COX-1, COX-2, PGI2S and microsomal PGES-1 (mPGES-1), and the production of PGE2 and PGI2 in human coronary artery endothelial cells (HCAEC). HCAEC monolayers were incubated with curcumin and the expression of mRNA, protein and the production of PGI2 and PGE2 were quantified. Incubation of HCAEC with curcumin led to a time and concentration-dependent increases in COX-2 mRNA with a small but significant decrease in COX-1 mRNA expression. Curcumin also stimulated the expression of PGI2S and mPGES-1 mRNA. Although curcumin stimulated COX-2, PGI2S and mPGES-1 gene expression, it failed to increase PGI2 or PGE2 production. Interestingly, supplementation of the culture medium with AA increased prostanoid production by both quiescent and curcumin-treated cells. However, in comparison to the quiescent cells, the prostanoid production by curcumin-treated cells was markedly enhanced as AA concentrations in the medium were increased, and the enhanced prostanoid production was blocked by the presence of COX-2 specific inhibitor. Taken together, these results suggest that curcumin regulates prostanoid homeostasis in HCAEC by modulating multiple steps including the expression of COX-1, COX-2, PGI2S and mPGES-1.

10

Involvement of hindbrain and peripheral prostanoids in gastric motor and cardiovascular responses to delta-9-tetrahydrocannabinol in the rat

58%

Krowicki Z. K.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 6

11

Vascular effects of COX inhibition and AT1 receptor blockade in transgenic rats harboring mouse renin-2 gene

58%

Cheng Z. J., Tikkanen I., Vapaatalo H., Mervaala E. M. A.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Ang II-induced endothelial dysfunction is associated with perivascular inflammation and increased superoxide production in the vascular wall. The present study examined the role of cyclo-oxygenase (COX)-synthetized eicosanoids in the pathogenesis of Ang II-induced endothelial dysfunction in transgenic rats harboring mouse renin-2 gene (mREN2 rats). Five-to-six-week-old, heterozygous mREN2 rats received the following drug regimens for 8 weeks: 1) vehicle, 2) cyclo-oxygenase-2 (COX-2) inhibitor (MF-tricyclic [3-(3,4-difluorophenyl)-4-(4-(methylsulfonyl) phenyl)-2(5H)-furanone], 14 mg/kg p.o.), 3) COX-l/COX-2 inhibitor (sulindac, 14 mg/kg p.o.), 4) angiotensin II receptor antagonist (losartan 40 mg/kg p.o.). Normotensive Sprague Dawley (SD) rats served as controls. In vitro vascular responses of the descending aorta and renal artery were studied using organ bath system. mREN2 rats developed pronounced hypertension which was associated with impaired endothelium-dependent and endothelium-independent vascular relaxations in the aorta. In contrast, the relaxation responses of the renal arteries remained largely unchanged in mREN2 rats. Urinary NOx excretion, a marker of total body NO generation, was also decreased in mREN2 rats. Neither non-selective COX inhibitor sulindac nor COX-2 selective MF-tricyclic were capable of preventing Ang II- induced hypertension or endothelial dysfunction in mREN2 rats, whereas ATi receptor antagonist losartan completely normalized blood pressure, vascular relaxation responses as well as urinary NOx excretion. Our findings indicate that NO synthesis and/or bioavailability as well as the sensitivity of arterial smooth muscle cells to NO are decreased in mREN2 rats. The present study also demonstrated that COX does not play a central role in the pathogenesis of Ang II-induced endothelial dysfunction in mREN2 rats.

12

Expression of cyclooxygenase-1 and cyclooxygenase-2 in normal and pathological human oral mucosa

51%

Mauro A., Lipari L., Leone A., Tortorici S., Burruano F., Provenzano S., Gerbino A., Buscemi M.

Folia Histochemica et Cytobiologica

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2010

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tom 48

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nr 4

Ograniczanie wyników

Control of the circulation by chemical mediators from the endothelium

Cyclooxygenase pathways

Prenatal exposure to hyperoxia modifies the thromboxane prostanoid receptor-mediated response to H2O2 in the ductus arteriosus of the chicken embryo

Labile products of vascular endothelium as mediators and modulators of the functions of the central nervous system

Actions and interactions of endothelins, prostacyclin and nitric oxide in the gastric mucosa

The role of cyclooxygenase [COX]-2 derived prostanoids on vasoconstrictor responses to phenylephrine is increased by exposure to low mercury concentration

Losartan inhibits the adhesion of rat platelets to fibrillar collagen - a potential role of nitric oxide and prostanoids

The effect of reactive oxygen species on the synthesis of prostanoids from arachidonic acid

Regulation of the expression of cyclooxygenases and production of prostaglandin I2 and E2 in human coronary artery endothelial cells by curcumin

Involvement of hindbrain and peripheral prostanoids in gastric motor and cardiovascular responses to delta-9-tetrahydrocannabinol in the rat

Vascular effects of COX inhibition and AT1 receptor blockade in transgenic rats harboring mouse renin-2 gene

Expression of cyclooxygenase-1 and cyclooxygenase-2 in normal and pathological human oral mucosa