β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands

Autores
Busch, Lucila; Sterin, Leonor Josefina; Borda, Enri Santiago
Año de publicación
2008
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
In this paper we have studied the influence of a well-established rat model of periodontitis on resting and adrenergic-stimulated mucin secretion from rat submandibular glands. The selective β1-receptor subtype agonist, dobutamine, induced mucin secretion while the selective β2-, α1- and α2-agonists, soterenol, phenylephrine and clonidine, respectively, did not. In rats subjected to ligature-induced periodontitis mucin release, under unstimulated conditions (basal values), was significantly increased. This increment was abolished in the presence of propranolol and atenolol. Isoproterenol, concentration-dependent, increased mucin release in control and in ligature-induced periodontitis rats. Maximal effect of isoproterenol was decreased in rats with ligature while EC50 was increased. Neither, the inhibition of NOS by l-NMMA nor the inhibition of COX by indomethacin could revert the effect of ligature on mucin release under unstimulated and isoproterenol-stimulated conditions. The inhibition of adenylyl cyclase by SQ 22536 resulted in a right shift of isoproterenol concentration-response curves in both groups, control and with ligature and returned basal values of rats with ligature to control ones. β-Receptor population was decreased in submandibular gland membranes from rats with ligature without changes in affinity. Potencies of the β-receptor antagonists in the competition studies were similar in both groups under study, control and with ligature. We conclude that in rats subjected to ligature-induced periodontitis unstimulated mucin secretion is increased. The increment seems to be due to an activation of the sympathetic system since it is inhibited by the β-adrenoceptors antagonists and by the inhibition of the adenylyl cyclase. We can speculate that inflammatory mediators from the experimental periodontitis could be involved in the mechanism underlying the activation of the sympathetic system.
Fil: Busch, Lucila. Universidad de Buenos Aires. Facultad de Odontología; Argentina
Fil: Sterin, Leonor Josefina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología; Argentina
Fil: Borda, Enri Santiago. Universidad de Buenos Aires. Facultad de Odontología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Materia
Β-RECEPTORS
MUCINE
PERIODONTITIS
SUBMANDIBULAR GLAND
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/160523

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oai_identifier_str oai:ri.conicet.gov.ar:11336/160523
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glandsBusch, LucilaSterin, Leonor JosefinaBorda, Enri SantiagoΒ-RECEPTORSMUCINEPERIODONTITISSUBMANDIBULAR GLANDhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3In this paper we have studied the influence of a well-established rat model of periodontitis on resting and adrenergic-stimulated mucin secretion from rat submandibular glands. The selective β1-receptor subtype agonist, dobutamine, induced mucin secretion while the selective β2-, α1- and α2-agonists, soterenol, phenylephrine and clonidine, respectively, did not. In rats subjected to ligature-induced periodontitis mucin release, under unstimulated conditions (basal values), was significantly increased. This increment was abolished in the presence of propranolol and atenolol. Isoproterenol, concentration-dependent, increased mucin release in control and in ligature-induced periodontitis rats. Maximal effect of isoproterenol was decreased in rats with ligature while EC50 was increased. Neither, the inhibition of NOS by l-NMMA nor the inhibition of COX by indomethacin could revert the effect of ligature on mucin release under unstimulated and isoproterenol-stimulated conditions. The inhibition of adenylyl cyclase by SQ 22536 resulted in a right shift of isoproterenol concentration-response curves in both groups, control and with ligature and returned basal values of rats with ligature to control ones. β-Receptor population was decreased in submandibular gland membranes from rats with ligature without changes in affinity. Potencies of the β-receptor antagonists in the competition studies were similar in both groups under study, control and with ligature. We conclude that in rats subjected to ligature-induced periodontitis unstimulated mucin secretion is increased. The increment seems to be due to an activation of the sympathetic system since it is inhibited by the β-adrenoceptors antagonists and by the inhibition of the adenylyl cyclase. We can speculate that inflammatory mediators from the experimental periodontitis could be involved in the mechanism underlying the activation of the sympathetic system.Fil: Busch, Lucila. Universidad de Buenos Aires. Facultad de Odontología; ArgentinaFil: Sterin, Leonor Josefina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología; ArgentinaFil: Borda, Enri Santiago. Universidad de Buenos Aires. Facultad de Odontología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaPergamon-Elsevier Science Ltd2008-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/160523Busch, Lucila; Sterin, Leonor Josefina; Borda, Enri Santiago; β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands; Pergamon-Elsevier Science Ltd; Archives of Oral Biology; 53; 6; 6-2008; 509-5160003-9969CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0003996908000022info:eu-repo/semantics/altIdentifier/doi/10.1016/j.archoralbio.2007.12.010info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:40:13Zoai:ri.conicet.gov.ar:11336/160523instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:40:13.272CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
title β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
spellingShingle β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
Busch, Lucila
Β-RECEPTORS
MUCINE
PERIODONTITIS
SUBMANDIBULAR GLAND
title_short β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
title_full β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
title_fullStr β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
title_full_unstemmed β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
title_sort β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands
dc.creator.none.fl_str_mv Busch, Lucila
Sterin, Leonor Josefina
Borda, Enri Santiago
author Busch, Lucila
author_facet Busch, Lucila
Sterin, Leonor Josefina
Borda, Enri Santiago
author_role author
author2 Sterin, Leonor Josefina
Borda, Enri Santiago
author2_role author
author
dc.subject.none.fl_str_mv Β-RECEPTORS
MUCINE
PERIODONTITIS
SUBMANDIBULAR GLAND
topic Β-RECEPTORS
MUCINE
PERIODONTITIS
SUBMANDIBULAR GLAND
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv In this paper we have studied the influence of a well-established rat model of periodontitis on resting and adrenergic-stimulated mucin secretion from rat submandibular glands. The selective β1-receptor subtype agonist, dobutamine, induced mucin secretion while the selective β2-, α1- and α2-agonists, soterenol, phenylephrine and clonidine, respectively, did not. In rats subjected to ligature-induced periodontitis mucin release, under unstimulated conditions (basal values), was significantly increased. This increment was abolished in the presence of propranolol and atenolol. Isoproterenol, concentration-dependent, increased mucin release in control and in ligature-induced periodontitis rats. Maximal effect of isoproterenol was decreased in rats with ligature while EC50 was increased. Neither, the inhibition of NOS by l-NMMA nor the inhibition of COX by indomethacin could revert the effect of ligature on mucin release under unstimulated and isoproterenol-stimulated conditions. The inhibition of adenylyl cyclase by SQ 22536 resulted in a right shift of isoproterenol concentration-response curves in both groups, control and with ligature and returned basal values of rats with ligature to control ones. β-Receptor population was decreased in submandibular gland membranes from rats with ligature without changes in affinity. Potencies of the β-receptor antagonists in the competition studies were similar in both groups under study, control and with ligature. We conclude that in rats subjected to ligature-induced periodontitis unstimulated mucin secretion is increased. The increment seems to be due to an activation of the sympathetic system since it is inhibited by the β-adrenoceptors antagonists and by the inhibition of the adenylyl cyclase. We can speculate that inflammatory mediators from the experimental periodontitis could be involved in the mechanism underlying the activation of the sympathetic system.
Fil: Busch, Lucila. Universidad de Buenos Aires. Facultad de Odontología; Argentina
Fil: Sterin, Leonor Josefina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología; Argentina
Fil: Borda, Enri Santiago. Universidad de Buenos Aires. Facultad de Odontología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
description In this paper we have studied the influence of a well-established rat model of periodontitis on resting and adrenergic-stimulated mucin secretion from rat submandibular glands. The selective β1-receptor subtype agonist, dobutamine, induced mucin secretion while the selective β2-, α1- and α2-agonists, soterenol, phenylephrine and clonidine, respectively, did not. In rats subjected to ligature-induced periodontitis mucin release, under unstimulated conditions (basal values), was significantly increased. This increment was abolished in the presence of propranolol and atenolol. Isoproterenol, concentration-dependent, increased mucin release in control and in ligature-induced periodontitis rats. Maximal effect of isoproterenol was decreased in rats with ligature while EC50 was increased. Neither, the inhibition of NOS by l-NMMA nor the inhibition of COX by indomethacin could revert the effect of ligature on mucin release under unstimulated and isoproterenol-stimulated conditions. The inhibition of adenylyl cyclase by SQ 22536 resulted in a right shift of isoproterenol concentration-response curves in both groups, control and with ligature and returned basal values of rats with ligature to control ones. β-Receptor population was decreased in submandibular gland membranes from rats with ligature without changes in affinity. Potencies of the β-receptor antagonists in the competition studies were similar in both groups under study, control and with ligature. We conclude that in rats subjected to ligature-induced periodontitis unstimulated mucin secretion is increased. The increment seems to be due to an activation of the sympathetic system since it is inhibited by the β-adrenoceptors antagonists and by the inhibition of the adenylyl cyclase. We can speculate that inflammatory mediators from the experimental periodontitis could be involved in the mechanism underlying the activation of the sympathetic system.
publishDate 2008
dc.date.none.fl_str_mv 2008-06
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/160523
Busch, Lucila; Sterin, Leonor Josefina; Borda, Enri Santiago; β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands; Pergamon-Elsevier Science Ltd; Archives of Oral Biology; 53; 6; 6-2008; 509-516
0003-9969
CONICET Digital
CONICET
url http://hdl.handle.net/11336/160523
identifier_str_mv Busch, Lucila; Sterin, Leonor Josefina; Borda, Enri Santiago; β-Adrenoceptor alterations coupled with secretory response and experimental periodontitis in rat submandibular glands; Pergamon-Elsevier Science Ltd; Archives of Oral Biology; 53; 6; 6-2008; 509-516
0003-9969
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0003996908000022
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.archoralbio.2007.12.010
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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