Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract

Detalhes bibliográficos
Autor(a) principal: Dias, ACR
Data de Publicação: 2005
Outros Autores: Vitela, M., Colombari, Eduardo [UNIFESP], Mifflin, S. W.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/28065
http://dx.doi.org/10.1152/ajpheart.01149.2003
Resumo: The neuromodulatory effect of NO on glutamatergic transmission has been studied in several brain areas. Our previous single-cell studies suggested that NO facilitates glutamatergic transmission in the nucleus of the solitary tract (NTS). in this study, we examined the effect of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on glutamatergic and reflex transmission in the NTS. We measured mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) from Inactin-anesthetized Sprague-Dawley rats. Bilateral microinjections of L-NAME (10 nmol/100 nl) into the NTS did not cause significant changes in basal MAP, HR, or RSNA. Unilateral microinjection of (RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 1 pmol/100 nl) into the NTS decreased MAP and RSNA. Fifteen minutes after L-NAME microinjections, AMPA-evoked cardiovascular changes were significantly reduced. N-methyl-D-aspartate (NMDA, 0.5 pmol/100 nl) microinjection into the NTS decreased MAP, HR, and RSNA. NMDA-evoked falls in MAP, HR, and RSNA were significantly reduced 30 min after L-NAME. To examine baroreceptor and cardiopulmonary reflex function, L-NAME was microinjected at multiple sites within the rostro-caudal extent of the NTS. Baroreflex function was tested with phenylephrine (PE, 25 mug iv) before and after L-NAME. Five minutes after L-NAME the decrease in RSNA caused by PE was significantly reduced. To examine cardiopulmonary reflex function, phenylbiguanide (PBG, 8 mug/kg) was injected into the right atrium. PBG-evoked hypotension, bradycardia, and RSNA reduction were significantly attenuated 5 min after L-NAME. Our results indicate that inhibition of NOS within the NTS attenuates baro- and cardiopulmonary reflexes, suggesting that NO plays a physiologically significant neuromodulatory role in cardiovascular regulation.
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spelling Dias, ACRVitela, M.Colombari, Eduardo [UNIFESP]Mifflin, S. W.Univ TexasUniversidade Federal de São Paulo (UNIFESP)2016-01-24T12:37:32Z2016-01-24T12:37:32Z2005-01-01American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 288, n. 1, p. H256-H262, 2005.0363-6135http://repositorio.unifesp.br/handle/11600/28065http://dx.doi.org/10.1152/ajpheart.01149.200310.1152/ajpheart.01149.2003WOS:000225733000037The neuromodulatory effect of NO on glutamatergic transmission has been studied in several brain areas. Our previous single-cell studies suggested that NO facilitates glutamatergic transmission in the nucleus of the solitary tract (NTS). in this study, we examined the effect of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on glutamatergic and reflex transmission in the NTS. We measured mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) from Inactin-anesthetized Sprague-Dawley rats. Bilateral microinjections of L-NAME (10 nmol/100 nl) into the NTS did not cause significant changes in basal MAP, HR, or RSNA. Unilateral microinjection of (RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 1 pmol/100 nl) into the NTS decreased MAP and RSNA. Fifteen minutes after L-NAME microinjections, AMPA-evoked cardiovascular changes were significantly reduced. N-methyl-D-aspartate (NMDA, 0.5 pmol/100 nl) microinjection into the NTS decreased MAP, HR, and RSNA. NMDA-evoked falls in MAP, HR, and RSNA were significantly reduced 30 min after L-NAME. To examine baroreceptor and cardiopulmonary reflex function, L-NAME was microinjected at multiple sites within the rostro-caudal extent of the NTS. Baroreflex function was tested with phenylephrine (PE, 25 mug iv) before and after L-NAME. Five minutes after L-NAME the decrease in RSNA caused by PE was significantly reduced. To examine cardiopulmonary reflex function, phenylbiguanide (PBG, 8 mug/kg) was injected into the right atrium. PBG-evoked hypotension, bradycardia, and RSNA reduction were significantly attenuated 5 min after L-NAME. Our results indicate that inhibition of NOS within the NTS attenuates baro- and cardiopulmonary reflexes, suggesting that NO plays a physiologically significant neuromodulatory role in cardiovascular regulation.Univ Texas, Hlth Sci Ctr, Dept Pharmacol, San Antonio, TX 78229 USAUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, BrazilWeb of ScienceH256-H262engAmer Physiological SocAmerican Journal of Physiology-heart and Circulatory Physiology(RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acidN-methyl-D aspartatebaroreceptor and cardiopulmonary reflexescardiovascular regulationrenal sympathetic nerve activityNitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tractinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/280652022-06-02 09:35:05.062metadata only accessoai:repositorio.unifesp.br:11600/28065Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:16:21.814321Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
title Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
spellingShingle Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
Dias, ACR
(RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid
N-methyl-D aspartate
baroreceptor and cardiopulmonary reflexes
cardiovascular regulation
renal sympathetic nerve activity
title_short Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
title_full Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
title_fullStr Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
title_full_unstemmed Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
title_sort Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
author Dias, ACR
author_facet Dias, ACR
Vitela, M.
Colombari, Eduardo [UNIFESP]
Mifflin, S. W.
author_role author
author2 Vitela, M.
Colombari, Eduardo [UNIFESP]
Mifflin, S. W.
author2_role author
author
author
dc.contributor.institution.none.fl_str_mv Univ Texas
Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Dias, ACR
Vitela, M.
Colombari, Eduardo [UNIFESP]
Mifflin, S. W.
dc.subject.eng.fl_str_mv (RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid
N-methyl-D aspartate
baroreceptor and cardiopulmonary reflexes
cardiovascular regulation
renal sympathetic nerve activity
topic (RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid
N-methyl-D aspartate
baroreceptor and cardiopulmonary reflexes
cardiovascular regulation
renal sympathetic nerve activity
description The neuromodulatory effect of NO on glutamatergic transmission has been studied in several brain areas. Our previous single-cell studies suggested that NO facilitates glutamatergic transmission in the nucleus of the solitary tract (NTS). in this study, we examined the effect of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on glutamatergic and reflex transmission in the NTS. We measured mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) from Inactin-anesthetized Sprague-Dawley rats. Bilateral microinjections of L-NAME (10 nmol/100 nl) into the NTS did not cause significant changes in basal MAP, HR, or RSNA. Unilateral microinjection of (RS)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 1 pmol/100 nl) into the NTS decreased MAP and RSNA. Fifteen minutes after L-NAME microinjections, AMPA-evoked cardiovascular changes were significantly reduced. N-methyl-D-aspartate (NMDA, 0.5 pmol/100 nl) microinjection into the NTS decreased MAP, HR, and RSNA. NMDA-evoked falls in MAP, HR, and RSNA were significantly reduced 30 min after L-NAME. To examine baroreceptor and cardiopulmonary reflex function, L-NAME was microinjected at multiple sites within the rostro-caudal extent of the NTS. Baroreflex function was tested with phenylephrine (PE, 25 mug iv) before and after L-NAME. Five minutes after L-NAME the decrease in RSNA caused by PE was significantly reduced. To examine cardiopulmonary reflex function, phenylbiguanide (PBG, 8 mug/kg) was injected into the right atrium. PBG-evoked hypotension, bradycardia, and RSNA reduction were significantly attenuated 5 min after L-NAME. Our results indicate that inhibition of NOS within the NTS attenuates baro- and cardiopulmonary reflexes, suggesting that NO plays a physiologically significant neuromodulatory role in cardiovascular regulation.
publishDate 2005
dc.date.issued.fl_str_mv 2005-01-01
dc.date.accessioned.fl_str_mv 2016-01-24T12:37:32Z
dc.date.available.fl_str_mv 2016-01-24T12:37:32Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.citation.fl_str_mv American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 288, n. 1, p. H256-H262, 2005.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/28065
http://dx.doi.org/10.1152/ajpheart.01149.2003
dc.identifier.issn.none.fl_str_mv 0363-6135
dc.identifier.doi.none.fl_str_mv 10.1152/ajpheart.01149.2003
dc.identifier.wos.none.fl_str_mv WOS:000225733000037
identifier_str_mv American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 288, n. 1, p. H256-H262, 2005.
0363-6135
10.1152/ajpheart.01149.2003
WOS:000225733000037
url http://repositorio.unifesp.br/handle/11600/28065
http://dx.doi.org/10.1152/ajpheart.01149.2003
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv American Journal of Physiology-heart and Circulatory Physiology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv H256-H262
dc.publisher.none.fl_str_mv Amer Physiological Soc
publisher.none.fl_str_mv Amer Physiological Soc
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv
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