A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats
Autor(a) principal: | |
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Data de Publicação: | 2012 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/34899 http://dx.doi.org/10.1371/journal.pone.0037587 |
Resumo: | Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. the purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280-350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free saporin (sham; 1.3 ng in 60 nl; n = 7). Two weeks later, the rats were anesthetized (urethane 1.2 g.kg(-1) b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. in sham rats, the HS infusion (3 M NaCl, 1.8 ml.kg(-1) b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9 +/- 2.7 mmHg) and increases in the RBF and RVC (141 +/- 7.9% and 140 +/- 7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (-45 +/- 5.0% at 10 min after HS) throughout the experimental period. in the A2-lesioned rats, the HS infusion induced transient hypertension (6 +/- 1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133 +/- 5.2% and 134 +/- 6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115 +/- 3.1% at 10 min after HS). the extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition. |
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Pedrino, Gustavo RodriguesFreiria-Oliveira, Andre HenriqueAlmeida Colombari, Debora SimoesRosa, Daniel AlvesCravo, Sergio Luiz [UNIFESP]Universidade Federal de Goiás (UFG)São Paulo State UnivUniversidade Federal de São Paulo (UNIFESP)2016-01-24T14:27:15Z2016-01-24T14:27:15Z2012-05-21Plos One. San Francisco: Public Library Science, v. 7, n. 5, 9 p., 2012.1932-6203http://repositorio.unifesp.br/handle/11600/34899http://dx.doi.org/10.1371/journal.pone.0037587WOS000305343100039.pdf10.1371/journal.pone.0037587WOS:000305343100039Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. the purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280-350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free saporin (sham; 1.3 ng in 60 nl; n = 7). Two weeks later, the rats were anesthetized (urethane 1.2 g.kg(-1) b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. in sham rats, the HS infusion (3 M NaCl, 1.8 ml.kg(-1) b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9 +/- 2.7 mmHg) and increases in the RBF and RVC (141 +/- 7.9% and 140 +/- 7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (-45 +/- 5.0% at 10 min after HS) throughout the experimental period. in the A2-lesioned rats, the HS infusion induced transient hypertension (6 +/- 1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133 +/- 5.2% and 134 +/- 6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115 +/- 3.1% at 10 min after HS). the extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG)Univ Fed Goias, Dept Physiol Sci, Goiania, Go, BrazilSão Paulo State Univ, Sch Dent, Dept Physiol & Pathol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, BrazilCAPES: BEX1380/07-9CNPq: 477832/2010-5Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG): 200910267000352Web of Science9engPublic Library SciencePlos OneA2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000305343100039.pdfapplication/pdf508458${dspace.ui.url}/bitstream/11600/34899/1/WOS000305343100039.pdfa7392830c82b358604527bd11df47fa4MD51open accessTEXTWOS000305343100039.pdf.txtWOS000305343100039.pdf.txtExtracted texttext/plain43288${dspace.ui.url}/bitstream/11600/34899/2/WOS000305343100039.pdf.txt81b35b413d5ee1961dcb5793beec1d3bMD52open access11600/348992022-02-18 10:09:40.595open accessoai:repositorio.unifesp.br:11600/34899Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:07:31.527465Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats |
title |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats |
spellingShingle |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats Pedrino, Gustavo Rodrigues |
title_short |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats |
title_full |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats |
title_fullStr |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats |
title_full_unstemmed |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats |
title_sort |
A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats |
author |
Pedrino, Gustavo Rodrigues |
author_facet |
Pedrino, Gustavo Rodrigues Freiria-Oliveira, Andre Henrique Almeida Colombari, Debora Simoes Rosa, Daniel Alves Cravo, Sergio Luiz [UNIFESP] |
author_role |
author |
author2 |
Freiria-Oliveira, Andre Henrique Almeida Colombari, Debora Simoes Rosa, Daniel Alves Cravo, Sergio Luiz [UNIFESP] |
author2_role |
author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de Goiás (UFG) São Paulo State Univ Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Pedrino, Gustavo Rodrigues Freiria-Oliveira, Andre Henrique Almeida Colombari, Debora Simoes Rosa, Daniel Alves Cravo, Sergio Luiz [UNIFESP] |
description |
Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. the purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280-350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free saporin (sham; 1.3 ng in 60 nl; n = 7). Two weeks later, the rats were anesthetized (urethane 1.2 g.kg(-1) b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. in sham rats, the HS infusion (3 M NaCl, 1.8 ml.kg(-1) b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9 +/- 2.7 mmHg) and increases in the RBF and RVC (141 +/- 7.9% and 140 +/- 7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (-45 +/- 5.0% at 10 min after HS) throughout the experimental period. in the A2-lesioned rats, the HS infusion induced transient hypertension (6 +/- 1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133 +/- 5.2% and 134 +/- 6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115 +/- 3.1% at 10 min after HS). the extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition. |
publishDate |
2012 |
dc.date.issued.fl_str_mv |
2012-05-21 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:27:15Z |
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2016-01-24T14:27:15Z |
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info:eu-repo/semantics/publishedVersion |
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article |
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dc.identifier.citation.fl_str_mv |
Plos One. San Francisco: Public Library Science, v. 7, n. 5, 9 p., 2012. |
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http://repositorio.unifesp.br/handle/11600/34899 http://dx.doi.org/10.1371/journal.pone.0037587 |
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1932-6203 |
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WOS000305343100039.pdf |
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10.1371/journal.pone.0037587 |
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WOS:000305343100039 |
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Plos One. San Francisco: Public Library Science, v. 7, n. 5, 9 p., 2012. 1932-6203 WOS000305343100039.pdf 10.1371/journal.pone.0037587 WOS:000305343100039 |
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http://repositorio.unifesp.br/handle/11600/34899 http://dx.doi.org/10.1371/journal.pone.0037587 |
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