A vaszkularis endoteliális növekedési faktor (VEGF) venulákra kifejtett hatásának vizsgálata patkány fogínyben.

Translated title of the contribution: [Investigation of the venodilatory effect of vascular endothelial growth factor (VEGF) in rat gingiva].

Milán Gyurkovics, Zs. Lohinai, Adrienne Gyorfi, D. Andrea Székely, E. Dinya, Arpád Fazekas, L. Rosivall

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

VEGF induces proliferation of endothelial cells, stimulates angiogenesis, and increases vascular permeability in many organs. Nevertheless, we have only limited information about its role on gingival hemodynamics, especially in venules. Therefor the aim of this study was to assess the acute circulatory effects of VEGF on rat gingival venules by means of the following protocol. Wister rats (n=63) were devided into five study groups after anesthesia; each animal received 10 microl of experimental solution dripped onto the lower interincisal gingiva. The groups included: 1) saline control (after the experiment, gingiva was excised for VEGF receptor 2 [VEGFR2] immunohistochemistry); 2) VEGF (0.1, 1, 10, or 50 microg/ml); 3) VEGF2 receptor antagonist 5-((7-benzyloxyquinazolin-4-yl)amino)-4-fluoro-2-methyl-phenol-hydrochloride (ZM323881; 20 microg/ml); 4) ZM323881 (20 microg/ml) followed by VEGF application (50 microg/ml after 15 minutes); and 5) VEGF (10 microg/ml), these rats were premedicated with nitric oxide (NO) synthase blocker (NG-nitro-L-arginine-methyl-ester [L-NAME]; 1 mg/ml in drinking water) for 1 week before the experiment. Changes in gingival superficial venule diameter were measured by vital microscopy prior to and 1, 5, 15, 30, and 60 minutes after the administration of the experimental solutions. According to our findings, VEGF dose-dependently increased the venular diameter compared to saline. ZM323881 alone did not cause any alteration. Premedication with ZM323881 or L-NAME decreased the dilatory effects of VEGF. Occassionally moderate VEGFR2 immunohistochemical labeling was observed in the wall components of the venules. Concluding our results we can say, that there is no remarkable VEGF production under physiologic circumstances in rat gingiva, but VEGF is able to increase gingival blood flow through the activation of VEGF2 receptors and consequent NO release.

Original languageHungarian
Pages (from-to)53-59
Number of pages7
JournalFogorvosi szemle
Volume106
Issue number2
Publication statusPublished - Jun 2013

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Gingiva
Vascular Endothelial Growth Factor A
Venules
NG-Nitroarginine Methyl Ester
Vascular Endothelial Growth Factor Receptor-2
Vascular Endothelial Growth Factor Receptor
Premedication
Capillary Permeability
Phenol
Nitric Oxide Synthase
Drinking Water
Microscopy
Anesthesia
Endothelial Cells
Hemodynamics
Immunohistochemistry
ZM323881

ASJC Scopus subject areas

  • Medicine(all)

Cite this

A vaszkularis endoteliális növekedési faktor (VEGF) venulákra kifejtett hatásának vizsgálata patkány fogínyben. / Gyurkovics, Milán; Lohinai, Zs.; Gyorfi, Adrienne; Székely, D. Andrea; Dinya, E.; Fazekas, Arpád; Rosivall, L.

In: Fogorvosi szemle, Vol. 106, No. 2, 06.2013, p. 53-59.

Research output: Contribution to journalArticle

Gyurkovics, Milán ; Lohinai, Zs. ; Gyorfi, Adrienne ; Székely, D. Andrea ; Dinya, E. ; Fazekas, Arpád ; Rosivall, L. / A vaszkularis endoteliális növekedési faktor (VEGF) venulákra kifejtett hatásának vizsgálata patkány fogínyben. In: Fogorvosi szemle. 2013 ; Vol. 106, No. 2. pp. 53-59.
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abstract = "VEGF induces proliferation of endothelial cells, stimulates angiogenesis, and increases vascular permeability in many organs. Nevertheless, we have only limited information about its role on gingival hemodynamics, especially in venules. Therefor the aim of this study was to assess the acute circulatory effects of VEGF on rat gingival venules by means of the following protocol. Wister rats (n=63) were devided into five study groups after anesthesia; each animal received 10 microl of experimental solution dripped onto the lower interincisal gingiva. The groups included: 1) saline control (after the experiment, gingiva was excised for VEGF receptor 2 [VEGFR2] immunohistochemistry); 2) VEGF (0.1, 1, 10, or 50 microg/ml); 3) VEGF2 receptor antagonist 5-((7-benzyloxyquinazolin-4-yl)amino)-4-fluoro-2-methyl-phenol-hydrochloride (ZM323881; 20 microg/ml); 4) ZM323881 (20 microg/ml) followed by VEGF application (50 microg/ml after 15 minutes); and 5) VEGF (10 microg/ml), these rats were premedicated with nitric oxide (NO) synthase blocker (NG-nitro-L-arginine-methyl-ester [L-NAME]; 1 mg/ml in drinking water) for 1 week before the experiment. Changes in gingival superficial venule diameter were measured by vital microscopy prior to and 1, 5, 15, 30, and 60 minutes after the administration of the experimental solutions. According to our findings, VEGF dose-dependently increased the venular diameter compared to saline. ZM323881 alone did not cause any alteration. Premedication with ZM323881 or L-NAME decreased the dilatory effects of VEGF. Occassionally moderate VEGFR2 immunohistochemical labeling was observed in the wall components of the venules. Concluding our results we can say, that there is no remarkable VEGF production under physiologic circumstances in rat gingiva, but VEGF is able to increase gingival blood flow through the activation of VEGF2 receptors and consequent NO release.",
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AU - Gyorfi, Adrienne

AU - Székely, D. Andrea

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