Endothelial. dysfunction in rats with ligature-induced periodontitis: Participation of nitric oxide and cycloxygenase-2-derived products
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Data
2016-03-01
Autores
Campi, Paula
Herrera, Bruno Schneider [UNESP]
Jesus, Flavia Neto de
Napolitano, Mauro
Teixeira, Simone Aparecida
Maia-Dantas, Aline
Spolidorio, Luis Carlos [UNESP]
Akamine, Eliana Hiromi
Alves Mayer, Marcia Pinto
Catelli de Carvalho, Maria Helena
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Editor
Elsevier B.V.
Resumo
Objectives: Considering the evident relationship between periodontitis and cardiovascular diseases in humans, we aimed to study the in vitro vascular reactivity of aorta rings prepared from rats with ligature induced periodontitis. Methods: Seven days after the induction of unilateral periodontitis, the animals were euthanised; rings were prepared from the descending abdominal aortas and mounted in tissue baths for the in vitro measurement of the isometric force responses to norepinephrine (NE) and acetylcholine (ACh), as well as in the presence of inhibitors of nitric oxide synthase (NOS) and cycloxygenase (COX) isoenzymes. Aortic COX and NOS gene expressions were analysed by RT-PCR, as well as protein COX-2 expression by Western blot. Results: Periodontitis resulted in significant alveolar bone loss and did not affect arterial pressure. However, both NE-induced contraction and ACh-induced relaxation were significantly decreased and related to the presence of endothelium. Diminished eNOS and augmented COX-2 and iNOS expressions were found in the aortas from rats with periodontitis, and the pharmacological inhibition of COX-2 or iNOS improved the observed vasomotor deficiencies. Conclusions: We can thus conclude that periodontitis induces significant endothelial dysfunction in rat aorta which is characterized by decreased eNOS expression and mediated by upregulated iNOS and COX 2 products. (C) 2015 Elsevier Ltd. All rights reserved.
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Palavras-chave
Periodontitis, Endothelium, Vascular, Aorta, Nitric oxide, Cyclooxygenase 2, Inflammation
Como citar
Archives Of Oral Biology. Oxford: Pergamon-elsevier Science Ltd, v. 63, p. 66-74, 2016.