Nitric oxide modulation of glutamatergic, baroreflex, and cardiopulmonary transmission in the nucleus of the solitary tract
Autor(a) principal: | |
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Data de Publicação: | 2005 |
Outros Autores: | , , |
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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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 |
|
_version_ |
1783460270263238656 |