The role of potassium channels in the endothelial dysfunction induced by periodontitis

Detalhes bibliográficos
Autor(a) principal: Olchanheski JR, Luiz Renato
Data de Publicação: 2022
Outros Autores: Sordi, Regina, Oliveira, Junior Garcia, Alves, Gustavo Ferreira, Mendes, Reila Taina, Santos, Fábio André, Fernandes, Daniel
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Journal of applied oral science (Online)
Texto Completo: https://www.revistas.usp.br/jaos/article/view/202966
Resumo: Objective: Periodontitis is associated with endothelial dysfunction, which is clinically characterized by a reduction in endothelium-dependent relaxation. However, we have previously shown that impairment in endothelium-dependent relaxation is transient. Therefore, we evaluated which mediators are involved in endothelium-dependent relaxation recovery. Material and methods: Rats were subjected to ligature-induced experimental periodontitis. Twenty-one days after the procedure, the animals were prepared for blood pressure recording, and the responses to acetylcholine or sodium nitroprusside were obtained before and 30 minutes after injection of a nitric oxide synthase inhibitor (L-NAME), cyclooxygenase inhibitor (Indomethacin, SC-550 and NS- 398), or calcium-dependent potassium channel blockers (apamin plus TRAM- 34). The maxilla and mandible were removed for bone loss analysis. Blood and gingivae were obtained for C-reactive protein (CRP) and myeloperoxidase (MPO) measurement, respectively. Results: Experimental periodontitis induces bone loss and an increase in the gingival MPO and plasmatic CRP. Periodontitis also reduced endothelium-dependent vasodilation, a hallmark of endothelial dysfunction, 14 days after the procedure. However, the response was restored at day 21. We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels. Conclusions: Periodontitis induces impairment in endothelial-dependent relaxation; this impairment recovers, even in the presence of periodontitis. The recovery is mediated by the activation of endothelial calcium-activated potassium channels in ligature animals. Although important for maintenance of vascular homeostasis, this effect could mask the lack of NO, which has other beneficial properties.
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spelling The role of potassium channels in the endothelial dysfunction induced by periodontitisEndotheliumNitric oxidePeriodontitisPotassium channelsObjective: Periodontitis is associated with endothelial dysfunction, which is clinically characterized by a reduction in endothelium-dependent relaxation. However, we have previously shown that impairment in endothelium-dependent relaxation is transient. Therefore, we evaluated which mediators are involved in endothelium-dependent relaxation recovery. Material and methods: Rats were subjected to ligature-induced experimental periodontitis. Twenty-one days after the procedure, the animals were prepared for blood pressure recording, and the responses to acetylcholine or sodium nitroprusside were obtained before and 30 minutes after injection of a nitric oxide synthase inhibitor (L-NAME), cyclooxygenase inhibitor (Indomethacin, SC-550 and NS- 398), or calcium-dependent potassium channel blockers (apamin plus TRAM- 34). The maxilla and mandible were removed for bone loss analysis. Blood and gingivae were obtained for C-reactive protein (CRP) and myeloperoxidase (MPO) measurement, respectively. Results: Experimental periodontitis induces bone loss and an increase in the gingival MPO and plasmatic CRP. Periodontitis also reduced endothelium-dependent vasodilation, a hallmark of endothelial dysfunction, 14 days after the procedure. However, the response was restored at day 21. We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels. Conclusions: Periodontitis induces impairment in endothelial-dependent relaxation; this impairment recovers, even in the presence of periodontitis. The recovery is mediated by the activation of endothelial calcium-activated potassium channels in ligature animals. Although important for maintenance of vascular homeostasis, this effect could mask the lack of NO, which has other beneficial properties.Universidade de São Paulo. Faculdade de Odontologia de Bauru2022-09-27info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/jaos/article/view/20296610.1590/1678-7757-2018-0048 Journal of Applied Oral Science; Vol. 26 (2018); e20170048Journal of Applied Oral Science; Vol. 26 (2018); e20170048Journal of Applied Oral Science; v. 26 (2018); e201700481678-77651678-7757reponame:Journal of applied oral science (Online)instname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/jaos/article/view/202966/187024Copyright (c) 2022 Journal of Applied Oral Sciencehttp://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessOlchanheski JR, Luiz RenatoSordi, Regina Oliveira, Junior GarciaAlves, Gustavo FerreiraMendes, Reila TainaSantos, Fábio AndréFernandes, Daniel2022-09-27T18:51:22Zoai:revistas.usp.br:article/202966Revistahttp://www.scielo.br/jaosPUBhttps://www.revistas.usp.br/jaos/oai||jaos@usp.br1678-77651678-7757opendoar:2022-09-27T18:51:22Journal of applied oral science (Online) - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv The role of potassium channels in the endothelial dysfunction induced by periodontitis
title The role of potassium channels in the endothelial dysfunction induced by periodontitis
spellingShingle The role of potassium channels in the endothelial dysfunction induced by periodontitis
Olchanheski JR, Luiz Renato
Endothelium
Nitric oxide
Periodontitis
Potassium channels
title_short The role of potassium channels in the endothelial dysfunction induced by periodontitis
title_full The role of potassium channels in the endothelial dysfunction induced by periodontitis
title_fullStr The role of potassium channels in the endothelial dysfunction induced by periodontitis
title_full_unstemmed The role of potassium channels in the endothelial dysfunction induced by periodontitis
title_sort The role of potassium channels in the endothelial dysfunction induced by periodontitis
author Olchanheski JR, Luiz Renato
author_facet Olchanheski JR, Luiz Renato
Sordi, Regina
Oliveira, Junior Garcia
Alves, Gustavo Ferreira
Mendes, Reila Taina
Santos, Fábio André
Fernandes, Daniel
author_role author
author2 Sordi, Regina
Oliveira, Junior Garcia
Alves, Gustavo Ferreira
Mendes, Reila Taina
Santos, Fábio André
Fernandes, Daniel
author2_role author
author
author
author
author
author
dc.contributor.author.fl_str_mv Olchanheski JR, Luiz Renato
Sordi, Regina
Oliveira, Junior Garcia
Alves, Gustavo Ferreira
Mendes, Reila Taina
Santos, Fábio André
Fernandes, Daniel
dc.subject.por.fl_str_mv Endothelium
Nitric oxide
Periodontitis
Potassium channels
topic Endothelium
Nitric oxide
Periodontitis
Potassium channels
description Objective: Periodontitis is associated with endothelial dysfunction, which is clinically characterized by a reduction in endothelium-dependent relaxation. However, we have previously shown that impairment in endothelium-dependent relaxation is transient. Therefore, we evaluated which mediators are involved in endothelium-dependent relaxation recovery. Material and methods: Rats were subjected to ligature-induced experimental periodontitis. Twenty-one days after the procedure, the animals were prepared for blood pressure recording, and the responses to acetylcholine or sodium nitroprusside were obtained before and 30 minutes after injection of a nitric oxide synthase inhibitor (L-NAME), cyclooxygenase inhibitor (Indomethacin, SC-550 and NS- 398), or calcium-dependent potassium channel blockers (apamin plus TRAM- 34). The maxilla and mandible were removed for bone loss analysis. Blood and gingivae were obtained for C-reactive protein (CRP) and myeloperoxidase (MPO) measurement, respectively. Results: Experimental periodontitis induces bone loss and an increase in the gingival MPO and plasmatic CRP. Periodontitis also reduced endothelium-dependent vasodilation, a hallmark of endothelial dysfunction, 14 days after the procedure. However, the response was restored at day 21. We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels. Conclusions: Periodontitis induces impairment in endothelial-dependent relaxation; this impairment recovers, even in the presence of periodontitis. The recovery is mediated by the activation of endothelial calcium-activated potassium channels in ligature animals. Although important for maintenance of vascular homeostasis, this effect could mask the lack of NO, which has other beneficial properties.
publishDate 2022
dc.date.none.fl_str_mv 2022-09-27
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/jaos/article/view/202966
10.1590/1678-7757-2018-0048
url https://www.revistas.usp.br/jaos/article/view/202966
identifier_str_mv 10.1590/1678-7757-2018-0048
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/jaos/article/view/202966/187024
dc.rights.driver.fl_str_mv Copyright (c) 2022 Journal of Applied Oral Science
http://creativecommons.org/licenses/by/4.0
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2022 Journal of Applied Oral Science
http://creativecommons.org/licenses/by/4.0
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Universidade de São Paulo. Faculdade de Odontologia de Bauru
publisher.none.fl_str_mv Universidade de São Paulo. Faculdade de Odontologia de Bauru
dc.source.none.fl_str_mv Journal of Applied Oral Science; Vol. 26 (2018); e20170048
Journal of Applied Oral Science; Vol. 26 (2018); e20170048
Journal of Applied Oral Science; v. 26 (2018); e20170048
1678-7765
1678-7757
reponame:Journal of applied oral science (Online)
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Journal of applied oral science (Online)
collection Journal of applied oral science (Online)
repository.name.fl_str_mv Journal of applied oral science (Online) - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||jaos@usp.br
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