Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio
Autor(a) principal: | |
---|---|
Data de Publicação: | 2014 |
Tipo de documento: | Tese |
Idioma: | por |
Título da fonte: | Repositório Institucional da UFSCAR |
Texto Completo: | https://repositorio.ufscar.br/handle/ufscar/1257 |
Resumo: | Sodium intake is induced by facilitatory signals, such as angiotensin II (ANG II) and aldosterone. Hyperosmolarity and central cholinergic activation, classic antinatriorexigenic stimuli, also induce NaCl intake when the inhibitory mechanisms of the lateral parabrachial nucleus (LPBN) are deactivated. In the present study, we investigated the possible interaction between osmoreceptors and cholinergic and angiotensinergic mechanisms in the control of water and NaCl intake induced by different dipsogenic and/or natriorexigenic stimuli combined with the blockade of LPBN inhibitory mechanisms. Rats with stainless steel cannulas implanted in the lateral ventricle (LV) or subfornical organ (SFO) and bilaterally into the LPBN were used to study the effects of injections of atropine (muscarinic cholinergic antagonist), losartan or ZD 7155 (AT1 receptor antagonists) into the LV or SFO on water and 0.3 M NaCl intake induced by bilateral injections of moxonidine (α2- adrenoceptor/imidazoline agonist) into the LPBN combined with a) plasma hyperosmolarity induced by intragastric (ig) 2 M NaCl; b) injections of carbachol (cholinergic agonist) into the LV or SFO; c) subcutaneous injections of furosemide (FURO) and captopril (CAP); d) injection of ANG II into the LV. Additionally, we also investigated whether acute application of osmotic, angiotensinergic and cholinergic stimuli would activate cultured SFO dissociated cells and if the same cell would be activated by different stimuli. In rats treated with ig 2 M NaCl, injections of moxonidine (0.5 nmol/0.2 μl) into the LPBN increased water and 0.3 M NaCl intake. Injections into the LV or SFO of atropine (20 nmol/1.0 μl and 2 nmol/0.1 μl, respectively) or losartan (100 μg/1.0 μl and 1 μg/0.1 μl, respectively) abolished water and 0.3 M NaCl intake in rats treated with ig 2 M NaCl combined with moxonidine into the LPBN. Moxonidine injected into the LPBN also increased water and 0.3 M NaCl intake induced by FURO + CAP, injections of ANG II (50 ng/1.0 μl) and carbachol (4 nmol/1.0 μl) into the LV or carbachol (0.5 nmol/0.1 μl) into the SFO. The blockade of AT1 receptors with injections of losartan into the LV or ZD 7155 (1 μg/0.1 μl) into the SFO abolished water and 0.3 M NaCl intake in rats treated with carbachol into the LV or SFO combined with LPBN injections of moxonidine. However, atropine injected into the LV, despite reducing water intake, did not change 0.3 M NaCl intake in rats treated with FURO + CAP or injection of ANG II into the LV combined with injections of moxonidine into the LPBN. Injections of losartan into the LV reduced 0.06 M sucrose intake, but did not change food intake induced by 24 h of food deprivation. Finally, in vitro studies showed that osmotic, angiotensinergic and cholinergic stimuli activate SFO dissociated cells and that different stimuli can activate the same SFO cell. Therefore, the results of the present study suggest that different stimuli, such as hyperosmolarity and central cholinergic activation, facilitate NaCl intake through activation of central angiotensinergic mechanisms. |
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Roncari, Camila FerreiraMenani, José Vanderleihttp://genos.cnpq.br:12010/dwlattes/owa/prc_imp_cv_int?f_cod=K4780462A5http://lattes.cnpq.br/07452530375262033b1f3bc8-e32b-42dd-8183-7a19395242752016-06-02T19:22:11Z2014-09-182016-06-02T19:22:11Z2014-08-26RONCARI, Camila Ferreira. Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio. 2014. 131 f. Tese (Doutorado em Ciências Biológicas) - Universidade Federal de São Carlos, São Carlos, 2014.https://repositorio.ufscar.br/handle/ufscar/1257Sodium intake is induced by facilitatory signals, such as angiotensin II (ANG II) and aldosterone. Hyperosmolarity and central cholinergic activation, classic antinatriorexigenic stimuli, also induce NaCl intake when the inhibitory mechanisms of the lateral parabrachial nucleus (LPBN) are deactivated. In the present study, we investigated the possible interaction between osmoreceptors and cholinergic and angiotensinergic mechanisms in the control of water and NaCl intake induced by different dipsogenic and/or natriorexigenic stimuli combined with the blockade of LPBN inhibitory mechanisms. Rats with stainless steel cannulas implanted in the lateral ventricle (LV) or subfornical organ (SFO) and bilaterally into the LPBN were used to study the effects of injections of atropine (muscarinic cholinergic antagonist), losartan or ZD 7155 (AT1 receptor antagonists) into the LV or SFO on water and 0.3 M NaCl intake induced by bilateral injections of moxonidine (α2- adrenoceptor/imidazoline agonist) into the LPBN combined with a) plasma hyperosmolarity induced by intragastric (ig) 2 M NaCl; b) injections of carbachol (cholinergic agonist) into the LV or SFO; c) subcutaneous injections of furosemide (FURO) and captopril (CAP); d) injection of ANG II into the LV. Additionally, we also investigated whether acute application of osmotic, angiotensinergic and cholinergic stimuli would activate cultured SFO dissociated cells and if the same cell would be activated by different stimuli. In rats treated with ig 2 M NaCl, injections of moxonidine (0.5 nmol/0.2 μl) into the LPBN increased water and 0.3 M NaCl intake. Injections into the LV or SFO of atropine (20 nmol/1.0 μl and 2 nmol/0.1 μl, respectively) or losartan (100 μg/1.0 μl and 1 μg/0.1 μl, respectively) abolished water and 0.3 M NaCl intake in rats treated with ig 2 M NaCl combined with moxonidine into the LPBN. Moxonidine injected into the LPBN also increased water and 0.3 M NaCl intake induced by FURO + CAP, injections of ANG II (50 ng/1.0 μl) and carbachol (4 nmol/1.0 μl) into the LV or carbachol (0.5 nmol/0.1 μl) into the SFO. The blockade of AT1 receptors with injections of losartan into the LV or ZD 7155 (1 μg/0.1 μl) into the SFO abolished water and 0.3 M NaCl intake in rats treated with carbachol into the LV or SFO combined with LPBN injections of moxonidine. However, atropine injected into the LV, despite reducing water intake, did not change 0.3 M NaCl intake in rats treated with FURO + CAP or injection of ANG II into the LV combined with injections of moxonidine into the LPBN. Injections of losartan into the LV reduced 0.06 M sucrose intake, but did not change food intake induced by 24 h of food deprivation. Finally, in vitro studies showed that osmotic, angiotensinergic and cholinergic stimuli activate SFO dissociated cells and that different stimuli can activate the same SFO cell. Therefore, the results of the present study suggest that different stimuli, such as hyperosmolarity and central cholinergic activation, facilitate NaCl intake through activation of central angiotensinergic mechanisms.A ingestão de sódio é induzida por sinais facilitatórios, como angiotensina II (ANG II) e aldosterona. A hiperosmolaridade e a estimulação colinérgica central, estímulos classicamente considerados antinatriorexigênicos, também induzem ingestão de NaCl quando os mecanismos inibitórios do núcleo parabraquial lateral (NPBL) são bloqueados. No presente estudo, investigamos a possível interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos centrais no controle da ingestão de água e NaCl induzida por diferentes estímulos dipsogênicos e/ou natriorexigênicos combinados com bloqueio dos mecanismos inibitórios do NPBL. Em ratos com cânulas de aço inoxidável implantadas no ventrículo lateral (VL) ou órgão subfornical (OSF) e bilateralmente no NPBL, foram estudados os efeitos de injeções de atropina (antagonista colinérgico muscarínico), losartan ou ZD 7155 (antagonistas de receptores AT1) no VL ou diretamente no OSF na ingestão de água e NaCl 0,3 M induzida por injeções bilaterais de moxonidina (agonista adrenérgico α2/imidazólico) no NPBL combinadas com: a) hiperosmolaridade plasmática induzida por sobrecarga intragástrica de NaCl 2 M; b) injeções de carbacol (agonista colinérgico) no VL ou OSF; c) injeções subcutâneas de furosemida (FURO) e captopril (CAP); d) injeção de ANG II no VL. Adicionalmente, também foi investigado se a aplicação aguda de estímulos osmóticos, angiotensinérgico e colinérgico ativariam neurônios dissociados do OSF mantidos em cultura e se um mesmo neurônio seria ativado por diferentes estímulos. Em ratos tratados com NaCl 2 M ig, injeções de moxonidina (0,5 nmol/0,2 μl) no NPBL aumentaram a ingestão de água e NaCl 0,3 M. Injeções no VL ou OSF de atropina (20 nmol/1,0 μl e 2 nmol/0,1 μl, respectivamente) ou losartan (100 μg/1,0 μl e 1 μg/0,1 μl, respectivamente) aboliram a ingestão de água e NaCl em ratos tratados com NaCl 2 M ig que receberam injeções de moxonidina no NPBL. Injeções de moxonidina também aumentaram a ingestão de água e NaCl 0,3 M induzida por FURO + CAP, injeções de ANG II (50 ng/1,0 μl) e carbacol (4 nmol/1,0 μl) no VL ou carbacol (0,5 nmol/0,1 μl) no OSF. O bloqueio de receptores AT1 com injeções de losartan no VL ou ZD 7155 (1 μg/0,1 μl) no OSF aboliu a ingestão de água e NaCl 0,3 M em ratos tratados com injeção de carbacol no VL ou OSF combinada com injeções de moxonidina no NPBL. No entanto, injeção de atropina no VL, apesar de reduzir a ingestão de água, não alterou a ingestão de NaCl 0,3 M em ratos tratados com FURO + CAP ou injeção de ANG II no VL combinados com injeções de moxonidina no NPBL. Injeções de losartan no VL reduziram a ingestão de sacarose 0,06 M, mas não alteraram a ingestão de ração induzida por privação alimentar por 24 h. Finalmente, os estudos in vitro mostraram que estímulos osmóticos, angiotensinérgico e colinérgico ativam as células dissociadas do OSF e que diferentes estímulos podem ativar uma mesma célula do OSF. Portanto, os resultados do presente estudo sugerem que diferentes estímulos, tais como hiperosmolaridade e ativação colinérgica central, facilitam a ingestão de NaCl através da ativação de mecanismos angiotensinérgicos centrais.Universidade Federal de Minas Geraisapplication/pdfporUniversidade Federal de São CarlosPrograma Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCFUFSCarBRFisiologiaNúcleo parabraquial lateralÓrgão subfornicalAngiotensina IICarbacolHiperosmolaridadeLateral parabrachial nucleusSubfornical organAngiotensin IIcarbacholHyperosmolarityCIENCIAS BIOLOGICAS::FISIOLOGIAInteração entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódioinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesis-1-1db436073-b604-4114-a5c8-76b09c26d760info:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFSCARinstname:Universidade Federal de São Carlos (UFSCAR)instacron:UFSCARORIGINAL6151.pdfapplication/pdf1975366https://repositorio.ufscar.br/bitstream/ufscar/1257/1/6151.pdf23b842452d75ee4bd80f5408eccc025cMD51TEXT6151.pdf.txt6151.pdf.txtExtracted texttext/plain0https://repositorio.ufscar.br/bitstream/ufscar/1257/2/6151.pdf.txtd41d8cd98f00b204e9800998ecf8427eMD52THUMBNAIL6151.pdf.jpg6151.pdf.jpgIM Thumbnailimage/jpeg8042https://repositorio.ufscar.br/bitstream/ufscar/1257/3/6151.pdf.jpgab721810c9c8d47c2b1980598a600560MD53ufscar/12572023-09-18 18:31:28.819oai:repositorio.ufscar.br:ufscar/1257Repositório InstitucionalPUBhttps://repositorio.ufscar.br/oai/requestopendoar:43222023-09-18T18:31:28Repositório Institucional da UFSCAR - Universidade Federal de São Carlos (UFSCAR)false |
dc.title.por.fl_str_mv |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio |
title |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio |
spellingShingle |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio Roncari, Camila Ferreira Fisiologia Núcleo parabraquial lateral Órgão subfornical Angiotensina II Carbacol Hiperosmolaridade Lateral parabrachial nucleus Subfornical organ Angiotensin II carbachol Hyperosmolarity CIENCIAS BIOLOGICAS::FISIOLOGIA |
title_short |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio |
title_full |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio |
title_fullStr |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio |
title_full_unstemmed |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio |
title_sort |
Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio |
author |
Roncari, Camila Ferreira |
author_facet |
Roncari, Camila Ferreira |
author_role |
author |
dc.contributor.authorlattes.por.fl_str_mv |
http://lattes.cnpq.br/0745253037526203 |
dc.contributor.author.fl_str_mv |
Roncari, Camila Ferreira |
dc.contributor.advisor1.fl_str_mv |
Menani, José Vanderlei |
dc.contributor.advisor1Lattes.fl_str_mv |
http://genos.cnpq.br:12010/dwlattes/owa/prc_imp_cv_int?f_cod=K4780462A5 |
dc.contributor.authorID.fl_str_mv |
3b1f3bc8-e32b-42dd-8183-7a1939524275 |
contributor_str_mv |
Menani, José Vanderlei |
dc.subject.por.fl_str_mv |
Fisiologia Núcleo parabraquial lateral Órgão subfornical Angiotensina II Carbacol Hiperosmolaridade |
topic |
Fisiologia Núcleo parabraquial lateral Órgão subfornical Angiotensina II Carbacol Hiperosmolaridade Lateral parabrachial nucleus Subfornical organ Angiotensin II carbachol Hyperosmolarity CIENCIAS BIOLOGICAS::FISIOLOGIA |
dc.subject.eng.fl_str_mv |
Lateral parabrachial nucleus Subfornical organ Angiotensin II carbachol Hyperosmolarity |
dc.subject.cnpq.fl_str_mv |
CIENCIAS BIOLOGICAS::FISIOLOGIA |
description |
Sodium intake is induced by facilitatory signals, such as angiotensin II (ANG II) and aldosterone. Hyperosmolarity and central cholinergic activation, classic antinatriorexigenic stimuli, also induce NaCl intake when the inhibitory mechanisms of the lateral parabrachial nucleus (LPBN) are deactivated. In the present study, we investigated the possible interaction between osmoreceptors and cholinergic and angiotensinergic mechanisms in the control of water and NaCl intake induced by different dipsogenic and/or natriorexigenic stimuli combined with the blockade of LPBN inhibitory mechanisms. Rats with stainless steel cannulas implanted in the lateral ventricle (LV) or subfornical organ (SFO) and bilaterally into the LPBN were used to study the effects of injections of atropine (muscarinic cholinergic antagonist), losartan or ZD 7155 (AT1 receptor antagonists) into the LV or SFO on water and 0.3 M NaCl intake induced by bilateral injections of moxonidine (α2- adrenoceptor/imidazoline agonist) into the LPBN combined with a) plasma hyperosmolarity induced by intragastric (ig) 2 M NaCl; b) injections of carbachol (cholinergic agonist) into the LV or SFO; c) subcutaneous injections of furosemide (FURO) and captopril (CAP); d) injection of ANG II into the LV. Additionally, we also investigated whether acute application of osmotic, angiotensinergic and cholinergic stimuli would activate cultured SFO dissociated cells and if the same cell would be activated by different stimuli. In rats treated with ig 2 M NaCl, injections of moxonidine (0.5 nmol/0.2 μl) into the LPBN increased water and 0.3 M NaCl intake. Injections into the LV or SFO of atropine (20 nmol/1.0 μl and 2 nmol/0.1 μl, respectively) or losartan (100 μg/1.0 μl and 1 μg/0.1 μl, respectively) abolished water and 0.3 M NaCl intake in rats treated with ig 2 M NaCl combined with moxonidine into the LPBN. Moxonidine injected into the LPBN also increased water and 0.3 M NaCl intake induced by FURO + CAP, injections of ANG II (50 ng/1.0 μl) and carbachol (4 nmol/1.0 μl) into the LV or carbachol (0.5 nmol/0.1 μl) into the SFO. The blockade of AT1 receptors with injections of losartan into the LV or ZD 7155 (1 μg/0.1 μl) into the SFO abolished water and 0.3 M NaCl intake in rats treated with carbachol into the LV or SFO combined with LPBN injections of moxonidine. However, atropine injected into the LV, despite reducing water intake, did not change 0.3 M NaCl intake in rats treated with FURO + CAP or injection of ANG II into the LV combined with injections of moxonidine into the LPBN. Injections of losartan into the LV reduced 0.06 M sucrose intake, but did not change food intake induced by 24 h of food deprivation. Finally, in vitro studies showed that osmotic, angiotensinergic and cholinergic stimuli activate SFO dissociated cells and that different stimuli can activate the same SFO cell. Therefore, the results of the present study suggest that different stimuli, such as hyperosmolarity and central cholinergic activation, facilitate NaCl intake through activation of central angiotensinergic mechanisms. |
publishDate |
2014 |
dc.date.available.fl_str_mv |
2014-09-18 2016-06-02T19:22:11Z |
dc.date.issued.fl_str_mv |
2014-08-26 |
dc.date.accessioned.fl_str_mv |
2016-06-02T19:22:11Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/doctoralThesis |
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publishedVersion |
dc.identifier.citation.fl_str_mv |
RONCARI, Camila Ferreira. Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio. 2014. 131 f. Tese (Doutorado em Ciências Biológicas) - Universidade Federal de São Carlos, São Carlos, 2014. |
dc.identifier.uri.fl_str_mv |
https://repositorio.ufscar.br/handle/ufscar/1257 |
identifier_str_mv |
RONCARI, Camila Ferreira. Interação entre osmorreceptores e mecanismos colinérgicos e angiotensinérgicos prosencefálicos no controle da ingestão de sódio. 2014. 131 f. Tese (Doutorado em Ciências Biológicas) - Universidade Federal de São Carlos, São Carlos, 2014. |
url |
https://repositorio.ufscar.br/handle/ufscar/1257 |
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Universidade Federal de São Carlos |
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Programa Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCF |
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UFSCar |
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BR |
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