Campi, PaulaHerrera, Bruno Schneider [UNESP]Jesus, Flavia Neto deNapolitano, MauroTeixeira, Simone AparecidaMaia-Dantas, AlineSpolidorio, Luis Carlos [UNESP]Akamine, Eliana HiromiAlves Mayer, Marcia PintoCatelli de Carvalho, Maria HelenaPereira Costa, Soraia KatiaMuscara, Marcelo Nicolas2018-11-262018-11-262016-03-01Archives Of Oral Biology. Oxford: Pergamon-elsevier Science Ltd, v. 63, p. 66-74, 2016.0003-9969http://hdl.handle.net/11449/161241Objectives: 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.66-74engPeriodontitisEndotheliumVascularAortaNitric oxideCyclooxygenase 2InflammationArtigo10.1016/j.archoralbio.2015.11.022WOS:000370833500009Acesso abertoWOS000370833500009.pdf2640929291808415