Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares
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| Data de Publicação: | 2016 |
| Tipo de documento: | Dissertação |
| Idioma: | por |
| Título da fonte: | Biblioteca Digital de Teses e Dissertações da UFRRJ |
| Texto Completo: | https://rima.ufrrj.br/jspui/handle/20.500.14407/11391 |
Resumo: | A regulação constante do balanço de água e sódio é essencial para a manutenção da vida. Desde os organismos mais simples até os mais complexos, a conservação de tais elementos em níveis adequados constitui ponto crucial para a homeostase do indivíduo. Para tanto, os organismos lançam mão de uma série de mecanismos neuro-humorais que regulam a todo momento o conteúdo de água e sódio corporal. Nas últimas décadas, estudos sobre mecanismos neurais envolvidos na regulação do apetite ao sódio têm ganhado destaque, uma vez que o consumo exagerado de cloreto de sódio está diretamente relacionado a alterações funcionais que podem gerar doenças como a hipertensão arterial. Além do alto consumo diário de sódio pelas sociedades ocidentais, há também um crescente número de casos de hipertensão arterial, particularmente do tipo denominado sal-sensível. Assim, é necessário que os mecanismos envolvidos nessas alterações sejam intensamente estudados em modelos científicos. Desta forma, através do uso de modelo animal, investigamos neste trabalho as alterações funcionais advindas da modificação do conteúdo de sódio presente na dieta dos animais. Para tanto, ratos Wistar machos foram randomicamente divididos em 4 grupos experimentais: i) controle (CTRL); ii) dieta pobre em sódio (DP); iii) furosemida (FURO); iv) sobrecarga salina (SS). A partir desta divisão, traçamos os perfis hidroeletrolítico, cardiovascular e molecular desses paradigmas de desafio ao balanço hidroeletrolítico. Verificamos que a dieta hipossódica e a furosemida foram capazes de induzir o apetite ao sódio de forma sustentada até 4 horas após reapresentação de fluidos (DP 4,1 ± 0,8 de peso corporal; FURO 8,5 ± 1,0 vs. CTRL 0,15 ± 0,08 mL/100g; p<0,05). Confirmamos a ocorrência de hipernatremia a partir da sobrecarga salina (SS 163,7 ± 1,6 vs. CTRL 143,2 ± 0,7 mEq/L; p<0,05) e, surpreendentemente, encontramos níveis natrêmicos maiores que o controle no grupo DP (DP 148,7 ± 1,8 vs. Ctrl 143,2 ± 0,7 mEq/L; p<0,05). Quanto à avaliação dos parâmetros cardíacos, somente o grupo furosemida apresentou PAM menor que o controle após a administração de fenilefrina nas concentrações de 10 e 50 μg/mL ( Phe10 = Furo 142,6 ± 19,1 vs. Ctrl 222,4 ± 14,2 ; Phe50 = Furo 261,0 ± 74,8 vs. Ctrl 190,9 ± 19,6 mmHg; p<0,05), provavelmente devido à hipovolemia nestes animais. Verificamos ainda que no grupo submetido à sobrecarga salina ocorre aumento da expressão de mRNA para AVP (SS 2,61 ± 0,16 vs. CTRL 1,04 ± 0,04 a.u - unidades arbitrárias; p<0,05) e OT (SS 1,52 ± 0,12 vs. CTRL 1,01 ± 0,05 a.u; p<0,05), enquanto que no grupo dieta pobre estes parâmetros são reduzidos (AVP - DP 0,65 ± 0,07vs. CTRL 1,04 ± 0,04; OT - DP 0,65 ± 0,06vs. CTRL 1,01 ± 0,05 a.u; p<0,05). Por fim, encontramos níveis aumentados de mRNA do receptor AT1 nos grupos sobrecarga salina (SS 2,94 ± 0,26 vs. CTRL 1,14 ± 0,25 a.u; p<0,05) e furosemida (Furo 3,08 ± 0,51 vs. CTRL 1,14 ± 0,25 a.u; p<0,05). Deste modo, estes resultados reforçam o importante papel dos sistemas neuroendócrinos centrais na modulação da homeostase hidroeletrolítica e cardiovascular |
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Monteiro, Lívia da Rocha NatalinoReis, Luis Carlos484.252.577-00http://lattes.cnpq.br/2679836949147357127.683.267-20http://lattes.cnpq.br/21076488500400722023-12-22T01:52:15Z2023-12-22T01:52:15Z2016-02-17MONTEIRO, Lívia da Rocha Natalino. Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares. 2016. 81 f. Dissertação (Mestrado em Ciências Fisiológicas) - Instituto de Ciências Biológicas e da Saúde, Universidade Federal Rural do Rio de Janeiro, Seropédica - RJ, 2016.https://rima.ufrrj.br/jspui/handle/20.500.14407/11391A regulação constante do balanço de água e sódio é essencial para a manutenção da vida. Desde os organismos mais simples até os mais complexos, a conservação de tais elementos em níveis adequados constitui ponto crucial para a homeostase do indivíduo. Para tanto, os organismos lançam mão de uma série de mecanismos neuro-humorais que regulam a todo momento o conteúdo de água e sódio corporal. Nas últimas décadas, estudos sobre mecanismos neurais envolvidos na regulação do apetite ao sódio têm ganhado destaque, uma vez que o consumo exagerado de cloreto de sódio está diretamente relacionado a alterações funcionais que podem gerar doenças como a hipertensão arterial. Além do alto consumo diário de sódio pelas sociedades ocidentais, há também um crescente número de casos de hipertensão arterial, particularmente do tipo denominado sal-sensível. Assim, é necessário que os mecanismos envolvidos nessas alterações sejam intensamente estudados em modelos científicos. Desta forma, através do uso de modelo animal, investigamos neste trabalho as alterações funcionais advindas da modificação do conteúdo de sódio presente na dieta dos animais. Para tanto, ratos Wistar machos foram randomicamente divididos em 4 grupos experimentais: i) controle (CTRL); ii) dieta pobre em sódio (DP); iii) furosemida (FURO); iv) sobrecarga salina (SS). A partir desta divisão, traçamos os perfis hidroeletrolítico, cardiovascular e molecular desses paradigmas de desafio ao balanço hidroeletrolítico. Verificamos que a dieta hipossódica e a furosemida foram capazes de induzir o apetite ao sódio de forma sustentada até 4 horas após reapresentação de fluidos (DP 4,1 ± 0,8 de peso corporal; FURO 8,5 ± 1,0 vs. CTRL 0,15 ± 0,08 mL/100g; p<0,05). Confirmamos a ocorrência de hipernatremia a partir da sobrecarga salina (SS 163,7 ± 1,6 vs. CTRL 143,2 ± 0,7 mEq/L; p<0,05) e, surpreendentemente, encontramos níveis natrêmicos maiores que o controle no grupo DP (DP 148,7 ± 1,8 vs. Ctrl 143,2 ± 0,7 mEq/L; p<0,05). Quanto à avaliação dos parâmetros cardíacos, somente o grupo furosemida apresentou PAM menor que o controle após a administração de fenilefrina nas concentrações de 10 e 50 μg/mL ( Phe10 = Furo 142,6 ± 19,1 vs. Ctrl 222,4 ± 14,2 ; Phe50 = Furo 261,0 ± 74,8 vs. Ctrl 190,9 ± 19,6 mmHg; p<0,05), provavelmente devido à hipovolemia nestes animais. Verificamos ainda que no grupo submetido à sobrecarga salina ocorre aumento da expressão de mRNA para AVP (SS 2,61 ± 0,16 vs. CTRL 1,04 ± 0,04 a.u - unidades arbitrárias; p<0,05) e OT (SS 1,52 ± 0,12 vs. CTRL 1,01 ± 0,05 a.u; p<0,05), enquanto que no grupo dieta pobre estes parâmetros são reduzidos (AVP - DP 0,65 ± 0,07vs. CTRL 1,04 ± 0,04; OT - DP 0,65 ± 0,06vs. CTRL 1,01 ± 0,05 a.u; p<0,05). Por fim, encontramos níveis aumentados de mRNA do receptor AT1 nos grupos sobrecarga salina (SS 2,94 ± 0,26 vs. CTRL 1,14 ± 0,25 a.u; p<0,05) e furosemida (Furo 3,08 ± 0,51 vs. CTRL 1,14 ± 0,25 a.u; p<0,05). Deste modo, estes resultados reforçam o importante papel dos sistemas neuroendócrinos centrais na modulação da homeostase hidroeletrolítica e cardiovascularFAPERJ - Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de JaneiroThe constant regulation of sodium and water balance is essential for the maintenance of life. From the simplest to the most complex organisms, conservation of such elements at appropriate levels is a vital issue for the homeostasis of the individual. In order to maintain this balance, organisms resort a set of neurohumoral mechanisms that constantly regulate the content of bodily water and sodium. In recent decades, studies of neural mechanisms involved in the regulation of sodium appetite have gained ground since the excessive intake of sodium chloride has been directly related to functional changes which can lead to diseases such as hypertension. Besides the high daily consumption of sodium chloride by occidental societies, there is also a growing number cases of hypertension, particularly the so-called “salt-sensitive”. Therefore, it is necessary that the mechanisms involved in these changes are intensively studied in scientific models. Thus, through the use of an animal model, we investigated the functional changes arising from the modification of sodium content in the diet of animals. Wistar male rats were randomly divided into 4 groups: i) control (CTRL); ii) low-sodium diet (LSD); iii) furosemide (FURO); iv) saline overload (SO). From this division, we draw the hydroelectrolytic, cardiovascular and molecular profiles of these paradigms four days after the protocols beginning. We found that low-sodium diet and furosemide were able to induce a sustained sodium appetite 4 hours after reintroduction of fluids when compared to control group (LSD: 4.1 ± 0.8 and FURO: 8.5 ± 1.0 vs. CTRL 0.15 ± 0.08 mL/100g body weight, p<0.05, respectively). Besides we have confirmed the occurrence of hypernatremia in SO group (163.7 ± 1.6 vs. 143.2 ± 0.7 mEq/L, p<0.05) we surprisingly have found higher plasma sodium levels in LSD (148.7 ± 1.0 vs. 143.2 ± 0.7 mEq/L, p<0.05) when compared to control group. During the assessment of cardiac parameters, only the FURO group showed smaller mean arterial pressure than control after administration of phenylephrine at both 10 and 50 μg/mL concentrations (Phe10: 142.6 ± 19.1 vs. 222.4 ± 14 bpm, p<0.05; Phe50: 261.0 ± 74.8 vs. 190.9 ± 19.6 mmHg, p<0.05, respectively), probably due to hypovolemia, a factor which could also explain the absence of hyponatremia in these animals. Concerning the molecular parameters within the PVN, SO group showed an increased mRNA expression of AVP (2.61 ± 0.16 vs. 1.04 ± 0.04 a.u., p<0.05) and OT (1.52 ± 0.12 vs. 1.01 ± 0.05 a.u., p<0.05), while in the LSD group, these parameters are reduced (AVP: 0.65 ± 0.07 vs. 1.04 ± 0.04 a.u., p<0.05; OT: 0.65 ± 0.06 vs. 1.01 ± 0.05 a.u., p<0.05), when compared to control group, respectively. Finally, we found increased levels of AT1 receptor mRNA in SO group (2.94 ± 0.26 vs. 1.14 ± 0.25 a.u, p<0.05) and FURO (3.08 ± 0.51 vs. 1.14 ± 0.25 a.u, p<0.05) compared to control, respectively. 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| dc.title.por.fl_str_mv |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares |
| dc.title.alternative.eng.fl_str_mv |
Protocols that defy the appetite to sodium: hydroelectrolytic, cardiovascular and molecular alterations |
| title |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares |
| spellingShingle |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares Monteiro, Lívia da Rocha Natalino Hydroectrolitic balance Sodium appetite Equilíbrio hidroeletrolítico. . Apetite ao sódio Alterações cardiovasculares Cardiovascular alterations Fisiologia |
| title_short |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares |
| title_full |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares |
| title_fullStr |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares |
| title_full_unstemmed |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares |
| title_sort |
Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares |
| author |
Monteiro, Lívia da Rocha Natalino |
| author_facet |
Monteiro, Lívia da Rocha Natalino |
| author_role |
author |
| dc.contributor.author.fl_str_mv |
Monteiro, Lívia da Rocha Natalino |
| dc.contributor.advisor1.fl_str_mv |
Reis, Luis Carlos |
| dc.contributor.advisor1ID.fl_str_mv |
484.252.577-00 |
| dc.contributor.advisor1Lattes.fl_str_mv |
http://lattes.cnpq.br/2679836949147357 |
| dc.contributor.authorID.fl_str_mv |
127.683.267-20 |
| dc.contributor.authorLattes.fl_str_mv |
http://lattes.cnpq.br/2107648850040072 |
| contributor_str_mv |
Reis, Luis Carlos |
| dc.subject.eng.fl_str_mv |
Hydroectrolitic balance Sodium appetite |
| topic |
Hydroectrolitic balance Sodium appetite Equilíbrio hidroeletrolítico. . Apetite ao sódio Alterações cardiovasculares Cardiovascular alterations Fisiologia |
| dc.subject.por.fl_str_mv |
Equilíbrio hidroeletrolítico. . Apetite ao sódio Alterações cardiovasculares Cardiovascular alterations |
| dc.subject.cnpq.fl_str_mv |
Fisiologia |
| description |
A regulação constante do balanço de água e sódio é essencial para a manutenção da vida. Desde os organismos mais simples até os mais complexos, a conservação de tais elementos em níveis adequados constitui ponto crucial para a homeostase do indivíduo. Para tanto, os organismos lançam mão de uma série de mecanismos neuro-humorais que regulam a todo momento o conteúdo de água e sódio corporal. Nas últimas décadas, estudos sobre mecanismos neurais envolvidos na regulação do apetite ao sódio têm ganhado destaque, uma vez que o consumo exagerado de cloreto de sódio está diretamente relacionado a alterações funcionais que podem gerar doenças como a hipertensão arterial. Além do alto consumo diário de sódio pelas sociedades ocidentais, há também um crescente número de casos de hipertensão arterial, particularmente do tipo denominado sal-sensível. Assim, é necessário que os mecanismos envolvidos nessas alterações sejam intensamente estudados em modelos científicos. Desta forma, através do uso de modelo animal, investigamos neste trabalho as alterações funcionais advindas da modificação do conteúdo de sódio presente na dieta dos animais. Para tanto, ratos Wistar machos foram randomicamente divididos em 4 grupos experimentais: i) controle (CTRL); ii) dieta pobre em sódio (DP); iii) furosemida (FURO); iv) sobrecarga salina (SS). A partir desta divisão, traçamos os perfis hidroeletrolítico, cardiovascular e molecular desses paradigmas de desafio ao balanço hidroeletrolítico. Verificamos que a dieta hipossódica e a furosemida foram capazes de induzir o apetite ao sódio de forma sustentada até 4 horas após reapresentação de fluidos (DP 4,1 ± 0,8 de peso corporal; FURO 8,5 ± 1,0 vs. CTRL 0,15 ± 0,08 mL/100g; p<0,05). Confirmamos a ocorrência de hipernatremia a partir da sobrecarga salina (SS 163,7 ± 1,6 vs. CTRL 143,2 ± 0,7 mEq/L; p<0,05) e, surpreendentemente, encontramos níveis natrêmicos maiores que o controle no grupo DP (DP 148,7 ± 1,8 vs. Ctrl 143,2 ± 0,7 mEq/L; p<0,05). Quanto à avaliação dos parâmetros cardíacos, somente o grupo furosemida apresentou PAM menor que o controle após a administração de fenilefrina nas concentrações de 10 e 50 μg/mL ( Phe10 = Furo 142,6 ± 19,1 vs. Ctrl 222,4 ± 14,2 ; Phe50 = Furo 261,0 ± 74,8 vs. Ctrl 190,9 ± 19,6 mmHg; p<0,05), provavelmente devido à hipovolemia nestes animais. Verificamos ainda que no grupo submetido à sobrecarga salina ocorre aumento da expressão de mRNA para AVP (SS 2,61 ± 0,16 vs. CTRL 1,04 ± 0,04 a.u - unidades arbitrárias; p<0,05) e OT (SS 1,52 ± 0,12 vs. CTRL 1,01 ± 0,05 a.u; p<0,05), enquanto que no grupo dieta pobre estes parâmetros são reduzidos (AVP - DP 0,65 ± 0,07vs. CTRL 1,04 ± 0,04; OT - DP 0,65 ± 0,06vs. CTRL 1,01 ± 0,05 a.u; p<0,05). Por fim, encontramos níveis aumentados de mRNA do receptor AT1 nos grupos sobrecarga salina (SS 2,94 ± 0,26 vs. CTRL 1,14 ± 0,25 a.u; p<0,05) e furosemida (Furo 3,08 ± 0,51 vs. CTRL 1,14 ± 0,25 a.u; p<0,05). Deste modo, estes resultados reforçam o importante papel dos sistemas neuroendócrinos centrais na modulação da homeostase hidroeletrolítica e cardiovascular |
| publishDate |
2016 |
| dc.date.issued.fl_str_mv |
2016-02-17 |
| dc.date.accessioned.fl_str_mv |
2023-12-22T01:52:15Z |
| dc.date.available.fl_str_mv |
2023-12-22T01:52:15Z |
| dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
| dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
| format |
masterThesis |
| status_str |
publishedVersion |
| dc.identifier.citation.fl_str_mv |
MONTEIRO, Lívia da Rocha Natalino. Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares. 2016. 81 f. Dissertação (Mestrado em Ciências Fisiológicas) - Instituto de Ciências Biológicas e da Saúde, Universidade Federal Rural do Rio de Janeiro, Seropédica - RJ, 2016. |
| dc.identifier.uri.fl_str_mv |
https://rima.ufrrj.br/jspui/handle/20.500.14407/11391 |
| identifier_str_mv |
MONTEIRO, Lívia da Rocha Natalino. Protocolos que desafiam o apetite ao sódio: alterações hidroeletrolíticas, cardiovasculares e moleculares. 2016. 81 f. Dissertação (Mestrado em Ciências Fisiológicas) - Instituto de Ciências Biológicas e da Saúde, Universidade Federal Rural do Rio de Janeiro, Seropédica - RJ, 2016. |
| url |
https://rima.ufrrj.br/jspui/handle/20.500.14407/11391 |
| dc.language.iso.fl_str_mv |
por |
| language |
por |
| dc.relation.references.por.fl_str_mv |
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