Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C

Detalhes bibliográficos
Ano de defesa: 2017
Autor(a) principal: Vieira, Brenna Lepaus Monteiro
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal do Espírito Santo
BR
Mestrado em Ciências Fisiológicas
Centro de Ciências da Saúde
UFES
Programa de Pós-Graduação em Ciências Fisiológicas
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
612
Link de acesso: http://repositorio.ufes.br/handle/10/7908
Resumo: Among the characteristics of renovascular hypertension we can highlight oxidative stress and endothelial dysfunction. Objective: To evaluate the effects of kefir on the endothelial dysfunction of rats with renovascular hypertension. Method: Wistar rats were divided into 3 groups Sham, 2K1C and 2K1C-Kefir treated for 60 days with Kefir (0.3ml/100g), by oral gavage. The arterial pressure was monitored during treatment through tail plethysmography and at the end of treatment the animals were submitted to direct PA recording. The aorta was used in the construction of dose-response curves to Acetylcholine (ACh), sodium nitroprusside (NPS), and Phenylephrine (Phe). Kidneys were removed and used for angiotensin I, II and 1-7 analysis and ACE (angiotensin converting enzyme) activity. Aortas were used for oxidative stress analysis using flow cytometry. Values indicate the mean ± SEM. * P <0.05 compared to the Sham group; # P <0.05 relative to the 2K1C group. RESULTS: The 2K1C group had higher SBP, DBP, MAP (203 ± 11, 129 ± 4, 179 ± 6 mmHg) than the sham group (139 ± 11, 67 ± 5, 94 ± 2). In the Kefir-treated rats the PAS, PAD and PAM decreased significantly when compared to the 2R1C group (180 ± 11, 89 ± 7, 128 ± 4 mmHg). The animals in the 2K1C group presented endothelial dysfunction, which was observed in the relaxation curve endothelium-dependent (Rmax: 56 ± 4% *) when compared to controls (Rmax: 85 ± 4%), and kefir treatment was able to reverse this dysfunction (Rmax: 72 ± 5% #). Vascular smooth muscle dysfunction was also observed in the NPS curve in the 2K1C group (Rmax: 87 ± 3% *) compared to the sham group (Rmax: 96 ± 2%), and kefir treatment failed to restore this dysfunction (Rmax: 90 ± 3%). The 2K1C group showed increased the response to phenylephrine (Rmax: 80 ± 2% *) when compared to sham group (Rmax: 73 ± 2%), and kefir treatment also did not decrease these responses in treated hypertensive animals (Rmax: 86 ± 3%). The role of NO and Prostanoids was verified by blocking with LNAME and Indomethacin and we observed that relaxation to ACh in 2R1C animals was decreased (dAUC: NO: 162 ± 9 *; Prostanoids Prostanoids: 86 ± 6 * au ) As compared to controls (dAUC: NO: 255 ± 11 *, Prostanoids: 29 ± 0.2 * au) and restored in kefir-treated animals (NO: 247 ± 8 #; Prostanoids: 54 ± 2% au). We also observed that ERO'S participation in the dysfunction of hypertensive animals (dAUC: dAUC: 92 ± 11 *), when compared with normotensive animals (dAUC: 1.2 ± 0.02), and similarly, kefir reestablished ERO levels in the treated animals (dAUC: 40 ± 6%). In the analysis of oxidative stress in the aorta and blood performed by flow cytometry, we observed that 2K1C animals showed an increase in the production of ROS in the blood (O-2: 1771 ± 32, H2O2: 562 ± 41 a.u) and in the aorta (O-2: 551 ± 42, H2O2: 929 ± 86 a.u) when compared to the sham group (• O-2: 251 ± 5, H2O2: 516 ± 60 a.u blood) (•O2: 1129 ± 85, H2O2: 191 ± 2 a.u aorta) and kefir treatment was able to decrease the production of these species in the blood (• O-2: 260 ± 60, H2O2: 370 ± 64 a.u) and in the aorta O-2: 1080 ± 70, H2O2: 198 ± 11 a.u). ACE activity was higher in serum (174 ± 11 nmol/min/ mg) and in the non-clipped kidney (0.48 ± 0.04 nmol/min/mg) of 2K1C rats when compared to the sham group (151 ± 6 nmol/min/mg serum and 0.35 ± 0.03 nmol/min/mg non-clipped kidney). Treatment with kefir decreased enzyme activity (148 ± 8 nmon/min/mg serum, 0.31 ± 0.01 nmol/min/mg non-clipped kidney). Therefore, we conclude that 60 days kefir treatment in rats with renovascular hypertension has several beneficial effects, attenuating hypertension, improving endothelial dysfunction and oxidative stress, as well as decreasing ACE activity.
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spelling Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1CRenovascular hypertensionEndothelial dysfunctionAngiotensin IIAngiotensin converting enzymeOxidative stressHipertensão renovascularKefirDisfunção endotelialAngiotensina IIEnzima conversora de angiotensinaEstresse oxidativoFisiologia612Among the characteristics of renovascular hypertension we can highlight oxidative stress and endothelial dysfunction. Objective: To evaluate the effects of kefir on the endothelial dysfunction of rats with renovascular hypertension. Method: Wistar rats were divided into 3 groups Sham, 2K1C and 2K1C-Kefir treated for 60 days with Kefir (0.3ml/100g), by oral gavage. The arterial pressure was monitored during treatment through tail plethysmography and at the end of treatment the animals were submitted to direct PA recording. The aorta was used in the construction of dose-response curves to Acetylcholine (ACh), sodium nitroprusside (NPS), and Phenylephrine (Phe). Kidneys were removed and used for angiotensin I, II and 1-7 analysis and ACE (angiotensin converting enzyme) activity. Aortas were used for oxidative stress analysis using flow cytometry. Values indicate the mean ± SEM. * P <0.05 compared to the Sham group; # P <0.05 relative to the 2K1C group. RESULTS: The 2K1C group had higher SBP, DBP, MAP (203 ± 11, 129 ± 4, 179 ± 6 mmHg) than the sham group (139 ± 11, 67 ± 5, 94 ± 2). In the Kefir-treated rats the PAS, PAD and PAM decreased significantly when compared to the 2R1C group (180 ± 11, 89 ± 7, 128 ± 4 mmHg). The animals in the 2K1C group presented endothelial dysfunction, which was observed in the relaxation curve endothelium-dependent (Rmax: 56 ± 4% *) when compared to controls (Rmax: 85 ± 4%), and kefir treatment was able to reverse this dysfunction (Rmax: 72 ± 5% #). Vascular smooth muscle dysfunction was also observed in the NPS curve in the 2K1C group (Rmax: 87 ± 3% *) compared to the sham group (Rmax: 96 ± 2%), and kefir treatment failed to restore this dysfunction (Rmax: 90 ± 3%). The 2K1C group showed increased the response to phenylephrine (Rmax: 80 ± 2% *) when compared to sham group (Rmax: 73 ± 2%), and kefir treatment also did not decrease these responses in treated hypertensive animals (Rmax: 86 ± 3%). The role of NO and Prostanoids was verified by blocking with LNAME and Indomethacin and we observed that relaxation to ACh in 2R1C animals was decreased (dAUC: NO: 162 ± 9 *; Prostanoids Prostanoids: 86 ± 6 * au ) As compared to controls (dAUC: NO: 255 ± 11 *, Prostanoids: 29 ± 0.2 * au) and restored in kefir-treated animals (NO: 247 ± 8 #; Prostanoids: 54 ± 2% au). We also observed that ERO'S participation in the dysfunction of hypertensive animals (dAUC: dAUC: 92 ± 11 *), when compared with normotensive animals (dAUC: 1.2 ± 0.02), and similarly, kefir reestablished ERO levels in the treated animals (dAUC: 40 ± 6%). In the analysis of oxidative stress in the aorta and blood performed by flow cytometry, we observed that 2K1C animals showed an increase in the production of ROS in the blood (O-2: 1771 ± 32, H2O2: 562 ± 41 a.u) and in the aorta (O-2: 551 ± 42, H2O2: 929 ± 86 a.u) when compared to the sham group (• O-2: 251 ± 5, H2O2: 516 ± 60 a.u blood) (•O2: 1129 ± 85, H2O2: 191 ± 2 a.u aorta) and kefir treatment was able to decrease the production of these species in the blood (• O-2: 260 ± 60, H2O2: 370 ± 64 a.u) and in the aorta O-2: 1080 ± 70, H2O2: 198 ± 11 a.u). ACE activity was higher in serum (174 ± 11 nmol/min/ mg) and in the non-clipped kidney (0.48 ± 0.04 nmol/min/mg) of 2K1C rats when compared to the sham group (151 ± 6 nmol/min/mg serum and 0.35 ± 0.03 nmol/min/mg non-clipped kidney). Treatment with kefir decreased enzyme activity (148 ± 8 nmon/min/mg serum, 0.31 ± 0.01 nmol/min/mg non-clipped kidney). Therefore, we conclude that 60 days kefir treatment in rats with renovascular hypertension has several beneficial effects, attenuating hypertension, improving endothelial dysfunction and oxidative stress, as well as decreasing ACE activity.Dentre as características da hipertensão renovascular podemos destacar o estresse oxidativo e a disfunção endotelial. Objetivo: avaliar efeitos do kefir na disfunção endotelial de ratos com hipertensão renovascular. Metodologia: Ratos Wistar foram divididos em 3 grupos Sham, 2R1C e 2R1C-Kefir tratados por 60 dias com Kefir (0,3ml/100g), por gavagem. A pressão dos animais foi acompanhada durante o tratamento através da pletismografia de cauda e ao final do tratamento os animais foram submetidos ao registro de PA direta. A aorta foi usada na construção de curvas dose-resposta à Acetilcolina (ACh) ou Nitroprussiato de sódio (NPS), e Fenilefrina (Phe). Os rins foram retirados e usados para dosagem de angiotensina I, II e 1-7 e atividade da ECA (Enzima conversora de angiotensina). As aortas e o sangue total foram usados na análise do estresse oxidativo usando a citometria de fluxo. Os valores indicam a média ± EPM. *P<0,05 em relação ao grupo Sham; # P<0,05 em relação ao grupo 2R1C. Resultados: O grupo 2R1C apresentou PAS, PAD, PAM (203±11, 129±4, 179 ± 6 mmHg) mais elevadas do que o grupo sham (139±11, 67±5, 94±2). Nos ratos tratados com Kefir a PAS, PAD e PAM diminuiu significativamente quando comparados com o grupo 2R1C (180±11, 89±7, 128±4 mmHg). Os animais do grupo 2R1C apresentaram disfunção endotelial, que foi observada na curva de relaxamento dependente do endotélio (Rmáx: 56±4%*) quando comparados aos controles (Rmáx: 85±4%), e o tratamento com kefir foi capaz de reverter essa disfunção (Rmáx: 72±5%#). Também foi observado disfunção do músculo liso vascular na curva de NPS no grupo 2R1C (Rmáx: 87±3%*) em relação ao grupo sham (Rmáx: 96±2%), e o tratamento com kefir não foi capaz de restaurar essa disfunção (Rmáx: 90±3%). O grupo 2R1C mostrou hiperreatividade (Rmáx: 80±2%*) na curva com Phe em relação ao grupo sham (Rmáx: 73±2%), e o tratamento com kefir também não diminuiu essa respostas nos animais hipertensos tratados (Rmáx: 86±3%). O papel do NO e dos prostanoides foi verificado realizando o bloqueio com L-NAME e Indometacina e observamos que o relaxamento à ACh nos animais 2R1C estavam diminuídos (dAUC: NO: 162 ± 9 *; Prostanoides: 86 ± 6* a.u ) quando comparados aos controles (dAUC: NO: 255 ± 11 *; Prostanoides: 29 ± 0,2* a.u) e foi restabelecido nos animais tratados (NO:247 ± 8#; Prostanoides: 54 ± 2# a.u). Observamos também que houve participação de EROs na disfunção dos animais hipertensos (dAUC: dAUC:92 ± 11*), quando comparados com os animais normotensos (dAUC: 1,2 ± 0,02), e semelhante o kefir restabeleceu os níveis de EROs nos animais tratados (dAUC: 40 ± 6#). Na análise do estresse oxidativo n aorta e no sangue realizado pela citometria de fluxo, observamos que os animais 2R1C apresentaram aumento na produção de EROs no sangue (O-2: 1771±32, H2O2: 562±41 a.u.) e na aorta (O-2: 551±42, H2O2: 929±86 a.u.) quando comparamos ao grupo sham (O-2: 251±5, H2O2: 516±60 a.u. sangue) (O-2: 1129 ± 85, H2O2: 191 ± 2 a.u aorta) e o tratamento com kefir foi capaz de promover diminuição da produção dessas espécies no sangue (O-2: 260±60, H2O2: 370±64 a.u.) e na aorta (O-2: 1080 ± 70, H2O2: 198 ± 11 a.u.). A atividade da ECA apresentou-se aumentada no soro (174±11 nmon/min/mg) e no rim não clipado (0,48±0,04 nmon/min/mg) de ratos 2R1C quando comparado com o grupo sham (151±6 nmon/min/mg soro e 0,35±0,03 nmon/min/mg rim não clipado). O tratamento com kefir diminuiu a atividade da enzima (148±8 nmon/min/mg soro; 0,31±0,01 nmon/min/mg rim não clipado). Logo, podemos concluir que o tratamento com kefir durante 60 dias em ratos com hipertensão renovascular apresenta vários efeitos benéficos, atenuando a hipertensão, melhorando a disfunção endotelial e o estresse oxidativo, como também diminuindo a atividade da ECA.Universidade Federal do Espírito SantoBRMestrado em Ciências FisiológicasCentro de Ciências da SaúdeUFESPrograma de Pós-Graduação em Ciências FisiológicasCampagnaro, Bianca PrandiVasquez, Elisardo CorralGava, Agata LagesPereira, Thiago de Melo CostaVieira, Brenna Lepaus Monteiro2018-08-01T22:58:29Z2018-08-012018-08-01T22:58:29Z2017-09-29info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisTextapplication/pdfhttp://repositorio.ufes.br/handle/10/7908porinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)instname:Universidade Federal do Espírito Santo (UFES)instacron:UFES2024-07-16T17:10:18Zoai:repositorio.ufes.br:10/7908Repositório InstitucionalPUBhttp://repositorio.ufes.br/oai/requestriufes@ufes.bropendoar:21082024-07-16T17:10:18Repositório Institucional da Universidade Federal do Espírito Santo (riUfes) - Universidade Federal do Espírito Santo (UFES)false
dc.title.none.fl_str_mv Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
title Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
spellingShingle Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
Vieira, Brenna Lepaus Monteiro
Renovascular hypertension
Endothelial dysfunction
Angiotensin II
Angiotensin converting enzyme
Oxidative stress
Hipertensão renovascular
Kefir
Disfunção endotelial
Angiotensina II
Enzima conversora de angiotensina
Estresse oxidativo
Fisiologia
612
title_short Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
title_full Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
title_fullStr Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
title_full_unstemmed Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
title_sort Efeitos do kefir na reatividade vascular de ratos com hipertensão renovascular 2R1C
author Vieira, Brenna Lepaus Monteiro
author_facet Vieira, Brenna Lepaus Monteiro
author_role author
dc.contributor.none.fl_str_mv Campagnaro, Bianca Prandi
Vasquez, Elisardo Corral
Gava, Agata Lages
Pereira, Thiago de Melo Costa
dc.contributor.author.fl_str_mv Vieira, Brenna Lepaus Monteiro
dc.subject.por.fl_str_mv Renovascular hypertension
Endothelial dysfunction
Angiotensin II
Angiotensin converting enzyme
Oxidative stress
Hipertensão renovascular
Kefir
Disfunção endotelial
Angiotensina II
Enzima conversora de angiotensina
Estresse oxidativo
Fisiologia
612
topic Renovascular hypertension
Endothelial dysfunction
Angiotensin II
Angiotensin converting enzyme
Oxidative stress
Hipertensão renovascular
Kefir
Disfunção endotelial
Angiotensina II
Enzima conversora de angiotensina
Estresse oxidativo
Fisiologia
612
description Among the characteristics of renovascular hypertension we can highlight oxidative stress and endothelial dysfunction. Objective: To evaluate the effects of kefir on the endothelial dysfunction of rats with renovascular hypertension. Method: Wistar rats were divided into 3 groups Sham, 2K1C and 2K1C-Kefir treated for 60 days with Kefir (0.3ml/100g), by oral gavage. The arterial pressure was monitored during treatment through tail plethysmography and at the end of treatment the animals were submitted to direct PA recording. The aorta was used in the construction of dose-response curves to Acetylcholine (ACh), sodium nitroprusside (NPS), and Phenylephrine (Phe). Kidneys were removed and used for angiotensin I, II and 1-7 analysis and ACE (angiotensin converting enzyme) activity. Aortas were used for oxidative stress analysis using flow cytometry. Values indicate the mean ± SEM. * P <0.05 compared to the Sham group; # P <0.05 relative to the 2K1C group. RESULTS: The 2K1C group had higher SBP, DBP, MAP (203 ± 11, 129 ± 4, 179 ± 6 mmHg) than the sham group (139 ± 11, 67 ± 5, 94 ± 2). In the Kefir-treated rats the PAS, PAD and PAM decreased significantly when compared to the 2R1C group (180 ± 11, 89 ± 7, 128 ± 4 mmHg). The animals in the 2K1C group presented endothelial dysfunction, which was observed in the relaxation curve endothelium-dependent (Rmax: 56 ± 4% *) when compared to controls (Rmax: 85 ± 4%), and kefir treatment was able to reverse this dysfunction (Rmax: 72 ± 5% #). Vascular smooth muscle dysfunction was also observed in the NPS curve in the 2K1C group (Rmax: 87 ± 3% *) compared to the sham group (Rmax: 96 ± 2%), and kefir treatment failed to restore this dysfunction (Rmax: 90 ± 3%). The 2K1C group showed increased the response to phenylephrine (Rmax: 80 ± 2% *) when compared to sham group (Rmax: 73 ± 2%), and kefir treatment also did not decrease these responses in treated hypertensive animals (Rmax: 86 ± 3%). The role of NO and Prostanoids was verified by blocking with LNAME and Indomethacin and we observed that relaxation to ACh in 2R1C animals was decreased (dAUC: NO: 162 ± 9 *; Prostanoids Prostanoids: 86 ± 6 * au ) As compared to controls (dAUC: NO: 255 ± 11 *, Prostanoids: 29 ± 0.2 * au) and restored in kefir-treated animals (NO: 247 ± 8 #; Prostanoids: 54 ± 2% au). We also observed that ERO'S participation in the dysfunction of hypertensive animals (dAUC: dAUC: 92 ± 11 *), when compared with normotensive animals (dAUC: 1.2 ± 0.02), and similarly, kefir reestablished ERO levels in the treated animals (dAUC: 40 ± 6%). In the analysis of oxidative stress in the aorta and blood performed by flow cytometry, we observed that 2K1C animals showed an increase in the production of ROS in the blood (O-2: 1771 ± 32, H2O2: 562 ± 41 a.u) and in the aorta (O-2: 551 ± 42, H2O2: 929 ± 86 a.u) when compared to the sham group (• O-2: 251 ± 5, H2O2: 516 ± 60 a.u blood) (•O2: 1129 ± 85, H2O2: 191 ± 2 a.u aorta) and kefir treatment was able to decrease the production of these species in the blood (• O-2: 260 ± 60, H2O2: 370 ± 64 a.u) and in the aorta O-2: 1080 ± 70, H2O2: 198 ± 11 a.u). ACE activity was higher in serum (174 ± 11 nmol/min/ mg) and in the non-clipped kidney (0.48 ± 0.04 nmol/min/mg) of 2K1C rats when compared to the sham group (151 ± 6 nmol/min/mg serum and 0.35 ± 0.03 nmol/min/mg non-clipped kidney). Treatment with kefir decreased enzyme activity (148 ± 8 nmon/min/mg serum, 0.31 ± 0.01 nmol/min/mg non-clipped kidney). Therefore, we conclude that 60 days kefir treatment in rats with renovascular hypertension has several beneficial effects, attenuating hypertension, improving endothelial dysfunction and oxidative stress, as well as decreasing ACE activity.
publishDate 2017
dc.date.none.fl_str_mv 2017-09-29
2018-08-01T22:58:29Z
2018-08-01
2018-08-01T22:58:29Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
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dc.identifier.uri.fl_str_mv http://repositorio.ufes.br/handle/10/7908
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dc.publisher.none.fl_str_mv Universidade Federal do Espírito Santo
BR
Mestrado em Ciências Fisiológicas
Centro de Ciências da Saúde
UFES
Programa de Pós-Graduação em Ciências Fisiológicas
publisher.none.fl_str_mv Universidade Federal do Espírito Santo
BR
Mestrado em Ciências Fisiológicas
Centro de Ciências da Saúde
UFES
Programa de Pós-Graduação em Ciências Fisiológicas
dc.source.none.fl_str_mv reponame:Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
instname:Universidade Federal do Espírito Santo (UFES)
instacron:UFES
instname_str Universidade Federal do Espírito Santo (UFES)
instacron_str UFES
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reponame_str Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
collection Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
repository.name.fl_str_mv Repositório Institucional da Universidade Federal do Espírito Santo (riUfes) - Universidade Federal do Espírito Santo (UFES)
repository.mail.fl_str_mv riufes@ufes.br
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