Wyniki wyszukiwania

1

Adenoviral expression of a C-terminal targeting region inhibits CADTK activation in vascular smooth muscle cells

100%

He Y., Kozlowski P., Li X., Mercatante D., Earp H. S., Graves L. M.

Cellular and Molecular Biology Letters

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1998

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tom 03

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nr 3

2

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Effects of glutamate and zinc ions on the contractility of vascular smooth muscle preparations

84%

Nguyen-Duong H.

Journal of Elementology

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2010

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tom 15

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nr 3

559-572

It was shown in this study that isolated porcine coronary arteries (PCA) contracted by depolarization with high Ko or by histamine are dose-dependently relaxed by glutamic acid, aspartic acid, N-methyl-asparate (NMDA) and γ-aminobutyric acid (GABA). Zn2+ was also shown to relax dose-dependently PCA contractions induced by 50 mM KCl with an ED50 value of about 1.5 mM and to inhibit dose-dependently histamine-induced contractions, shifting ED50 values from 6μM to 40 μM, not affecting however corresponding cumulative concentration-response (CCR) curves established for acetylcholine-induced contractions. Furthermore, since Zn2+ ions are co-localized in many glutamatergic synapses of the central nervous system, it has been postulated in analogy to glutamate neurotoxicity that perturbations of the synaptic zinc concentrations might be a triggering factor in several cerebral diseases, such as ischemic strokes and sustained seizures. Unfortunately, little is known so far about effects of glutamate and zinc ions on the vascular tone. Although the nature of the glutamatergic receptors occurring in the blood vessels investigated in this study remains unclear, the results suggest that glutamate and Zn2+ ions interact with voltage-gated as well with ligand-operated Ca-channels. An interesting aspect might be the putative role of glutamate and zinc as long-term toxic agents in the early steps of the pathomechanisms leading to degenerative vascular lesions.

3

Reversal of the postischaemic suppression of coronary function in perfused guinea pig heart by ischaemic preconditioning

84%

Chlopicki S., Lomnicka M., Gryglewski R. J.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 4

4

Ligands of peroxisome proliferator-activated receptor-gamma increase the generation of vascular endothelial growth factor in vascular smooth muscle cells and in macrophages

84%

Jozkowicz A., Dulak J., Piatkowska E., Placha W., Dembinska-Kiec A.

Acta Biochimica Polonica

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2000

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tom 47

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nr 4

Peroxisome proliferator-activated receptors-gamma (PPARgamma) are ligand-inducible transcription factors of the nuclear hormone receptor superfamily. We examined the effect of PPARgamma activation on the generation of vascular endothelial growth factor (VEGF), one of the major angiogenic agents. Rat vascular smooth muscle cells (VSMC) and murine macrophages RAW264.7 were incubated for 24 h with PPARgamma activators: prostaglandin J2 and ciglitazone. PPARgamma were expressed in VSMC and RAW cells and their activity was upregulated in the presence of PGJ2 and ciglitazone. Incubation of the cells with PPARgamma activators significantly augmented the release of VEGF protein into the media, both in resting and in IL-1beta- or LPS-stimulated cultures. The higher protein generation was connected with the increased expression of mRNA and transcriptional activation of VEGF promoter. We conclude that the activation of PPARgamma upregulates the generation of VEGF and may be involved in the regulation of angiogenesis.

5

Is bradykinin [BK] a physiological vasodilator in the gut?

84%

Jacobson E. D., Berguer R., Higgins A., Stewart J. M.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 4

6

Inhibitors of nitric oxide synthesis and ischemia-reperfusion attenuate coronary vasodilator response to pinacidil in isolated rat heart

67%

Maczewski M., Beresewicz A.

Journal of Physiology and Pharmacology

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1997

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tom 48

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nr 4

7

Cysteinyl-leukotriene receptors in pulmonary vessels

67%

Walch L., Norel X., Gascard J. P., Brink C.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 4

8

Nitric oxide mediates the mitogenic effects of insulin and vascular endothelial growth factor but not of leptin in endothelial cells

67%

Jozkowicz A., Pankiewicz J., Dulak J., Partyka L., Wybranska I., Huk I., Dembinska-Kiec A.

Acta Biochimica Polonica

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1999

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tom 46

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nr 3

The regulation of vascular wall homeostasis by nitric oxide (NO) generated by endothelium is being intensively studied. In the present paper, the involvement of NO in the vascular endothelial growth factor (VEGF), insulin or leptin-stimulated proliferation of human endothelial cells (HUVEC) was measured by [3H]thymidine or bromodeoxyuridine incorporation. VEGF and insulin, but not leptin, increased NO generation in HUVEC, as detected with ISO-NO electrode. Proliferation of HUVEC induced by leptin was not changed or was higher in the presence of L-Nω-nitro-L-arginine methyl ester (L-NAME) a nitric oxide synthase (NOS) inhibitor. In contrast, L-NAME blunted the proproliferative effect of VEGF and insulin. Furthermore, we demonstrated that, in human arterial smooth muscle cells (hASMC) transfected with endothelial NOS (eNOS) gene, the generation of biologically active VEGF protein was NO-dependent. Inhibition of NO generation by L-NAME decreased the synthesis of VEGF protein and attenuated HUVEC proliferation induced by conditioned media from transfected hASMC. Endothelium-derived NO seems to participate in VEGF and insulin, but not leptin, mitogenic activity. Additionally, the small amounts of NO released from endothelial cells, as mimicked by eNOS transfection into hASMC, may activate generation of VEGF in sub-endothelial smooth muscle cells, leading to increased synthesis of VEGF protein necessary for turnover and restitution of endothelial cells.

Ograniczanie wyników

Adenoviral expression of a C-terminal targeting region inhibits CADTK activation in vascular smooth muscle cells

Effects of glutamate and zinc ions on the contractility of vascular smooth muscle preparations

Reversal of the postischaemic suppression of coronary function in perfused guinea pig heart by ischaemic preconditioning

Ligands of peroxisome proliferator-activated receptor-gamma increase the generation of vascular endothelial growth factor in vascular smooth muscle cells and in macrophages

Is bradykinin [BK] a physiological vasodilator in the gut?

Inhibitors of nitric oxide synthesis and ischemia-reperfusion attenuate coronary vasodilator response to pinacidil in isolated rat heart

Cysteinyl-leukotriene receptors in pulmonary vessels

Nitric oxide mediates the mitogenic effects of insulin and vascular endothelial growth factor but not of leptin in endothelial cells