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Id: lil-662371
Autor: Ma, Li-kun; Li, Qian; He, Li-feng; Hua, Jin-sheng; Zhou, Jun-ling; Yu, Hua; Feng, Ke-fu; Chen, Hong-wu; Hu, Hao; Wang, Lin.
Título: Imatinib atenua a fibrose miocárdica em associação com a inibição da atividade do PDGFRα / Imatinib attenuates myocardial fibrosis in association with inhibition of the PDGFRα activity
Fonte: Arq. bras. cardiol;99(6):1082-1091, dez. 2012. ilus, graf, tab.
Idioma: pt.
Resumo: FUNDAMENTO: O Imatinib é um inibidor do receptor tirosina-quinase que foi confirmada como exercendo um efeito inibidor sobre a atividade do receptor do PDGF, fator de crescimento plaquetário (PDGFRα e PDGFRβ). OBJETIVO: Investigar o efeito protetor do Imatinib na fibrose miocárdica em acetato de deoxicorticosterona (DOCA)/ratos com hipertensão induzida por sal. MÉTODOS: Sessenta ratos Sprague-Dawley machos, uninefrectomizados foram distribuídos em três grupos: ratos controles (grupo CON): grupo deoxicorticosterona (grupo DOCA); grupo deoxicorticosterona e Imatinib (grupo DOCA IMA). A Pressão Arterial Sistólica (PAS) foi medida quinzenalmente. Foi estudada a porção apical do ventrículo esquerdo. Foram empregados: coloração vermelho sirius, coloração de hematoxilina-eosina, imuno-histoquímica e ensaio de western blot. RESULTADOS: A PAS nos grupos DOCA e IMA+DOCA foi maior que no grupo CON nos dias 14 e 28. Os animais do grupo DOCA apresentaram fibrose intersticial e perivascular grave no dia 28, e as expressões de PI, PIII, tenascina-C e fibronectina foram significativamente maiores que nos grupos DOCA+IMA e CON. Quando comparados com o grupo CON, os grupos DOCA e DOCA+IMA apresentaram resposta inflamatória de tecido miocárdico e infiltração de monócitos/macrófagos de diferentes graus. As expressões proteicas do PDGF-A, PDGF-C e PDGFRα foram significativamente maiores nos grupos DOCA e DOCA+IMA que no grupo CON, mas a expressão proteica do p-PDGFRα no grupo DOCA+IMA foi menor que no DOCA. CONCLUSÃO: O Imatinib pode exercer efeitos inibitórios sobre a fibrose miocárdica em ratos com hipertensão induzida por DOCA/sal, os quais podem ser atribuídos à inibição da atividade do PDGFR-α.

BACKGROUND: Imatinib is a tyrosine kinase receptor inhibitor that has been confirmed to exert inhibitory effect on the platelet derived growth factor PDGF receptor (PDGFRα and PDGFRβ) activity. OBJECTIVE: To investigate the protective effect of imatinib on the myocardial fibrosis in deoxycorticosterone-acetate (DOCA)/salt induced hypertensive rats. METHODS: Sixty male uninephrectomized Sprague-Dawley rats were assigned to three groups: control rats (CON group); deoxycorticosterone group (DOCA group); deoxycorticosterone and imatinib group (DOCA+IMA group). Systolic blood pressure (SBP) was measured biweekly. The apical portion of the left ventricle was studied. Sirius-Red staining, Hematoxylin-Eosin staining, immunohistochemistry and Western blot assay were employed. RESULTS: SBP in the DOCA group and DOCA+IMA group was higher than that in the CON group on day 14 and 28. Animals in the DOCA group showed severe interstitial and perivascular fibrosis on day 28, and the expressions of PI, PIII, tenascin-C and fibronectin were significantly higher than those in the DOCA+IMA group and CON group. When compared with the CON group, myocardial tissue inflammatory response and monocyte/macrophage infiltration of different degrees were observed in the DOCA group and DOCA+IMA group. Protein expressions of PDGF-A, PDGF-C and PDGFRα were signiflcantly higher in the DOCA and DOCA+IMA groups than those in the CON group, but the p-PDGFRα protein expression in the DOCA+IMA group was lower than that in the DOCA group. CONCLUSION: Imatinib can exert inhibitory effects on myocardial fibrosis in DOCA/salt induced hypertensive rats, which may be attributed to the inhibition of PDGFR-α activity.
Descritores: Benzamidas/farmacologia
Fibrose Endomiocárdica/tratamento farmacológico
Piperazinas/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
-Western Blotting
Benzamidas/uso terapêutico
Pressão Sanguínea/efeitos dos fármacos
Desoxicorticosterona
Modelos Animais de Doenças
Fibrose Endomiocárdica/patologia
Fibronectinas/análise
Fibronectinas/metabolismo
Fibrose/tratamento farmacológico
Fibrose/patologia
Hipertensão/induzido quimicamente
Hipertensão/fisiopatologia
Nefrectomia/métodos
Piperazinas/uso terapêutico
Inibidores de Proteínas Quinases/uso terapêutico
Pirimidinas/uso terapêutico
Ratos Sprague-Dawley
Receptor alfa de Fator de Crescimento Derivado de Plaquetas/metabolismo
Receptor beta de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Resultado do Tratamento
Tenascina/análise
Tenascina/metabolismo
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


  2 / 21 LILACS  
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Id: lil-626346
Autor: Moreira, Cleci M.; Meira, Eduardo F.; Vestena, Luis; Stefanon, Ivanita; Vassallo, Dalton V.; Padilha, Alessandra S..
Título: Tension cost correlates with mechanical and biochemical parameters in different myocardial contractility conditions
Fonte: Clinics;67(5):489-496, 2012. graf, tab.
Idioma: en.
Resumo: OBJECTIVES: Tension cost, the ratio of myosin ATPase activity to tension, reflects the economy of tension development in the myocardium. To evaluate the mechanical advantage represented by the tension cost, we studied papillary muscle contractility and the activity of myosin ATPase in the left ventricles in normal and pathophysiological conditions. METHODS: Experimental protocols were performed using rat left ventricles from: (1) streptozotocin-induced diabetic and control Wistar rats; (2) N-nitro-L-arginine methyl ester (L-NAME) hypertensive and untreated Wistar rats; (3) deoxycorticosterone acetate (DOCA) salt-treated, nephrectomized and salt- and DOCA-treated rats; (4) spontaneous hypertensive rats (SHR) and Wistar Kyoto (WKY) rats; (5) rats with myocardial infarction and shamoperated rats. The isometric force, tetanic tension, and the activity of myosin ATPase were measured. RESULTS: The results obtained from infarcted, diabetic, and deoxycorticosterone acetate-salt-treated rats showed reductions in twitch and tetanic tension compared to the control and sham-operated groups. Twitch and tetanic tension increased in the N-nitro-L-arginine methyl ester-treated rats compared with the Wistar rats. Myosin ATPase activity was depressed in the infarcted, diabetic, and deoxycorticosterone acetate salt-treated rats compared with control and sham-operated rats and was increased in N-nitro-L-arginine methyl ester-treated rats. These parameters did not differ between SHR and WKY rats. In the studied conditions (e.g., post-myocardial infarction, deoxycorticosterone acetate salt-induced hypertension, chronic N-nitro-L-arginine methyl ester treatment, and streptozotocin-induced diabetes), a positive correlation between force or plateau tetanic tension and myosin ATPase activity was observed. CONCLUSION: Our results suggest that the myocardium adapts to force generation by increasing or reducing the tension cost to maintain myocardial contractility with a better mechanical advantage.
Descritores: Diabetes Mellitus Experimental/fisiopatologia
Hipertensão/fisiopatologia
Contração Miocárdica/fisiologia
Infarto do Miocárdio/fisiopatologia
Músculos Papilares/fisiopatologia
Função Ventricular Esquerda
Miosinas Ventriculares/metabolismo
-Desoxicorticosterona/análogos & derivados
Diabetes Mellitus Experimental/induzido quimicamente
Inibidores Enzimáticos
Hipertensão/induzido quimicamente
Contração Miocárdica/efeitos dos fármacos
Nefrectomia
NG-Nitroarginina Metil Éster
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Limites: Animais
Masculino
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  3 / 21 LILACS  
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Id: lil-471321
Autor: Barbosa, Adriana Dias Elpo; Morato, Gina Struffaldi.
Título: Influence of epipregnanolone on the modulation of rapid tolerance to ethanol by neurosteroids
Fonte: Rev. bras. psiquiatr;29(4):337-345, dez. 2007. tab.
Idioma: en.
Resumo: OBJECTIVE: The objective of the present study was to investigate the effect of epipregnanolone on the influence of neurosteroids on the development of rapid tolerance to the motor impairing and hypothermic effects of ethanol. METHOD: Experiment 1: on Day 1 groups of mice were pretreated with saline or with epipregnanolone. After 30 min each group was further divided in subgroups that received ethanol or saline. Thirty, 60 and 90 min after the injections the animals were tested on the rota-rod or the body temperature was measured. On Day 2 all groups received ethanol and a similar procedure was followed to evaluate rapid tolerance. Experiment 2 and 3: On Day 1 groups of mice were treated with epipregnanolone and after 15 min each group was divided into three groups in order to receive pregnenolone sulfate, dehydroepiandrosterone sulfate or saline. Thirty minutes later, each group was further divided into two subgroups in order to receive ethanol or saline, respectively, and 30, 60 and 90 min later the animals were tested as in the experiment 1. On Day 2 all groups received ethanol and a similar procedure was followed to evaluate rapid tolerance. RESULTS: Pretreatment with epipregnanolone (0.10-0.30 mg/kg) significantly blocked the development of tolerance to the motor impairing and hypothermic effects induced by ethanol in mice. Considering tolerance to ethanol-induced motor impairment, epipregnanolone (0.15 mg/kg) reversed the stimulatory action of dehydroepiandrosterone sulfate (0.15 mg/kg), but did not affect the actions of pregnenolone sulfate (0.08 mg/kg). Moreover, epipregnanolone prevented the inhibitory action of allotetrahydrodeoxycorticosterone (0.10 mg/kg). In relation to ethanol-induced hypothermia, the results showed that pretreatment with epipregnanolone (0.30 mg/kg) significantly prevented the stimulatory action of dehydroepiandrosterone sulfate and pregnenolone sulfate, as well as the inhibitory action of...

OBJETIVO: O objetivo do presente estudo foi o de investigar o efeito da epipregnanolona sobre a influência de neuroesteróides no desenvolvimento da tolerância rápida aos efeitos de incoordenação motora e hipotermia induzidos pelo etanol. MÉTODO: Experimento 1: no Dia 1, grupos de camundongos foram pré-tratados com salina ou com epipregnanolona. Após 30 min, cada grupo foi subdividido recebendo etanol ou salina. Aos 30, 60 e 90 min após as injeções, os animais foram testados no rota-rod ou a temperatura corporal foi avaliada. No Dia 2, todos os grupos receberam etanol e um procedimento similar foi seguido para avaliar a tolerância rápida. O pré-tratamento com a epipregnanolona (0,10-0,30 mg/kg) bloqueou significantemente o desenvolvimento da tolerância aos efeitos de incoordenação motora e hipotermia induzidos pelo etanol em camundongos. Experimento 2 e 3: no Dia 1, grupos de animais foram tratados com epipregnanolona e, após 15 min, cada grupo foi dividido em três grupos para receber sulfato de pregnanolona, sulfato de dehidroepiandrosterona ou salina. Após 30 min, cada grupo foi dividido em dois subgrupos para receber etanol ou salina, respectivamente, e após 30, 60 e 90 min os animais foram testados como no experimento 1. No Dia 2, todos os grupos receberam etanol e 30 min após foram testados como mencionado no experimento 1. RESULTADOS: Considerando a tolerância ao prejuízo motor induzido pelo etanol, a epipregnanolona (0,15 mg/kg) bloqueou a ação estimulatória do sulfato de dehidroepiandrosterona (0,15 mg/kg), mas não afetou a ação do sulfato de pregnanolona (0,08 mg/kg). Entretanto, a epipregnanolona bloqueou a ação inibitória da alotetrahidrodeoxicorticosterona (0,10 mg/kg). Em relação à hipotermia induzida pelo etanol, os resultados demonstraram que o pré-tratamento com epipregnanolona (0,30 mg/kg) bloqueou significantemente a ação estimulatória do sulfato de dehidroepiandrosterona e do sulfato de pregnanolona, bem como a ação...
Descritores: Anestésicos/farmacologia
Depressores do Sistema Nervoso Central/farmacologia
Etanol/farmacologia
Hipotermia/induzido quimicamente
Atividade Motora/efeitos dos fármacos
Pregnanolona/farmacologia
-Análise de Variância
Temperatura Corporal/efeitos dos fármacos
Modelos Animais de Doenças
Avaliação Pré-Clínica de Medicamentos
Interações Medicamentosas
Tolerância a Medicamentos
Desoxicorticosterona/análogos & derivados
Desoxicorticosterona/farmacologia
Pregnenolona/farmacologia
Limites: Animais
Masculino
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  4 / 21 LILACS  
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Rudge, Marilza V. C
Calderon, Iracema M. P
Id: lil-339848
Autor: Borges, Vera T. M; Rudge, Marilza V. C; Matsubara, Beatriz M; Calderon, Iracema M. P.
Título: Mecanismos envolvidos na adaptação cardiocirculatória durante a gravidez / Mechanisms involved in cardiocirculatory adaptation during pregnancy
Fonte: Femina;26(5):423-426, jun. 1998.
Idioma: pt.
Descritores: Aldosterona
Fator Natriurético Atrial
Complicações Cardiovasculares na Gravidez/fisiopatologia
Desoxicorticosterona
Taxa de Filtração Glomerular
Hemodinâmica/genética
Fatores Físicos e Químicos
-Débito Cardíaco
Frequência Cardíaca
Limites: Humanos
Feminino
Gravidez
Responsável: BR1365.1 - Biblioteca Biomédica A - CB/A


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Reboucas, N. A
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Id: lil-325901
Autor: David, F. L; Montezano, A. C. I; Rebouças, N. A; Nigro, D; Fortes, Z. B; Carvalho, M. H. C; Tostes, R. C. A.
Título: Gender differences in vascular expression of endothelin and ET A/ET B receptors, but not in calcium handling mechanisms, in deoxycorticosterone acetate-salt hypertension
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;35(9):1061-1068, Sept. 2002. ilus, graf.
Idioma: en.
Conferência: Apresentado em: International Symposium on Vasoactive Peptides, 4, Belo Horizonte, Oct. 19-21, 2001.
Resumo: We determined if the increased vascular responsiveness to endothelin-1 (ET-1) observed in male, but not in female, DOCA-salt rats is associated with differential vascular mRNA expression of ET-1 and/or ET A/ET B receptors or with functional differences in Ca2+ handling mechanisms by vascular myocytes. Uninephrectomized male and female Wistar rats received DOCA and drinking water containing NaCl/KCl. Control rats received vehicle and tap water. Blood pressure and contractile responses of endothelium-denuded aortic rings to agents which induce Ca2+ influx and/or its release from internal stores were measured using standard procedures. Expression of mRNA for ET-1 and ET A/ET B receptors was evaluated by RT-PCR after isolation of total cell RNA from both aorta and mesenteric arteries. Systolic blood pressure was higher in male than in female DOCA rats. Contractions induced by Bay K8644 (which activates Ca2+ influx through voltage-operated L-type channels), and by caffeine, serotonin or ET-1 in Ca2+-free buffer (which reflect Ca2+ release from internal stores) were significantly increased in aortas from male and female DOCA-salt compared to control aortas. DOCA-salt treatment of male, but not female, rats statistically increased vascular mRNA expression of ET-1 and ET B receptors, but decreased the expression of ET A receptors. Molecular up-regulation of vascular ET B receptors, rather than differential changes in smooth muscle Ca2+ handling mechanisms, seems to account for the increased vascular reactivity to ET-1/ET B receptor agonists and higher blood pressure levels observed in male DOCA-salt rats
Descritores: Desoxicorticosterona
Endotelina-1
Hipertensão
Receptores de Endotelina
Cloreto de Sódio
Vasoconstrição
-Ratos Wistar
Reação em Cadeia da Polimerase Via Transcriptase Reversa
RNA Mensageiro
Caracteres Sexuais
Limites: Animais
Masculino
Feminino
Ratos
Responsável: BR1.1 - BIREME


  6 / 21 LILACS  
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Id: lil-325898
Autor: Watson, R. E; Supowit, S. C; Zhao, H; Katki, K. A; Dipette, D. J.
Título: Role of sensory nervous system vasoactive peptides in hypertension
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;35(9):1033-1045, Sept. 2002. ilus, tab, graf.
Idioma: en.
Conferência: Apresentado em: International Symposium on Vasoactive Peptides, 4, Belo Horizonte, Oct. 19-21, 2001.
Projeto: National Institutes of Health.
Resumo: The goal of the present research was to elucidate the roles and mechanisms by which the sensory nervous system, through the actions of potent vasodilator neuropeptides, regulates cardiovascular function in both the normal state and in the pathophysiology of hypertension. The animal models of acquired hypertension studied were deoxycorticosterone-salt (DOC-salt), subtotal nephrectomy-salt (SN-salt), and Nomega-nitro-L-arginine methyl ester (L-NAME)-induced hypertension during pregnancy in rats. The genetic model was the spontaneously hypertensive rat (SHR). Calcitonin gene-related peptide (CGRP) and substance P (SP) are potent vasodilating neuropeptides. In the acquired models of hypertension, CGRP and SP play compensatory roles to buffer the blood pressure (BP) increase. Their synthesis and release are increased in the DOC-salt model but not in the SN-salt model. This suggests that the mechanism by which both models lower BP in SN-salt rats is by increased vascular sensitivity. CGRP functions in a similar manner in the L-NAME model. In the SHR, synthesis of CGRP and SP is decreased. This could contribute to the BP elevation in this model. The CGRP gene knockout mouse has increased baseline mean arterial pressure. The long-term synthesis and release of CGRP is increased by nerve growth factor, bradykinin, and prostaglandins and is decreased by alpha2-adrenoreceptor agonists and glucocorticoids. In several animal models, sensory nervous system vasoactive peptides play a role in chronic BP elevation. In the acquired models, they play a compensatory role. In the genetic model, their decreased levels may contribute to the elevated BP. The roles of CGRP and SP in human hypertension are yet to be clarified
Descritores: Peptídeo Relacionado com Gene de Calcitonina
Hipertensão
Substância P
-Pressão Sanguínea
Peptídeo Relacionado com Gene de Calcitonina
Desoxicorticosterona
Modelos Animais de Doenças
Hipertensão
NG-Nitroarginina Metil Éster
Substância P
Limites: Animais
Feminino
Gravidez
Camundongos
Ratos
Tipo de Publ: Revisão
Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


  7 / 21 LILACS  
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Vassallo, D. V
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Id: lil-290156
Autor: Rossoni, L. V; Pinto, V. D; Vassallo, D. V.
Título: Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;34(8):1065-1077, Aug. 2001. ilus, tab.
Idioma: en.
Resumo: Ouabain increases vascular resistance and may induce hypertension by inhibiting the Na+ pump. The effects of 0.18 and 18 æg/kg, and 1.8 mg/kg ouabain pretreatment on the phenylephrine (PHE; 0.1, 0.25 and 0.5 æg, in bolus)-evoked pressor responses were investigated using anesthetized normotensive (control and uninephrectomized) and hypertensive (1K1C and DOCA-salt treated) rats. Treatment with 18 æg/kg ouabain increased systolic and diastolic blood pressure in all groups studied. However, the magnitude of this increase was larger for the hypertensive 1K1C and DOCA-salt rats than for normotensive animals, while the pressor effect of 0.18 æg/kg ouabain was greater only in DOCA-salt rats. A very large dose (1.8 mg/kg) produced toxic effects on the normotensive control but not on uninephrectomized or 1K1C rats. Rat tail vascular beds were perfused to analyze the effects of 10 nM ouabain on the pressor response to PHE. In all animals, 10 nM ouabain increased the PHE pressor response, but this increase was larger in hypertensive DOCA-salt rats than in normotensive and 1K1C rats. Results suggested that a) increases in diastolic blood pressure induced by 18 æg/kg ouabain were larger in hypertensive than normotensive rats; b) in DOCA-salt rats, smaller ouabain doses had a stronger effect than in other groups; c) hypertensive and uninephrectomized rats were less sensitive to toxic doses of ouabain, and d) after treatment with 10 nM ouabain isolated tail vascular beds from DOCA-salt rats were more sensitive to the pressor effect of PHE than those from normotensive and 1K1C hypertensive rats. These data suggest that very small doses of ouabain, which might produce nanomolar plasma concentrations, enhance pressor reactivity in DOCA-salt hypertensive rats, supporting the idea that endogenous ouabain may contribute to the increase and maintenance of vascular tone in hypertension
Descritores: Pressão Sanguínea/efeitos dos fármacos
Cardiotônicos/administração & dosagem
Hipertensão/tratamento farmacológico
Ouabaína/administração & dosagem
Fenilefrina/farmacologia
Vasoconstrição/efeitos dos fármacos
-Análise de Variância
Desoxicorticosterona
Modelos Animais de Doenças
Hipertensão Renovascular/metabolismo
Hipertensão/fisiopatologia
Ratos Wistar
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


  8 / 21 LILACS  
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Id: lil-284124
Autor: Fazan Júnior, Rubens; Silva, Valdo José Dias da; Salgado, Helio Cesar.
Título: Modelos de hipertensäo arterial / Experimental models of arterial hypertension
Fonte: Rev. bras. hipertens;8(1):19-29, jan.-mar. 2001. ilus.
Idioma: pt.
Resumo: Existe uma busca extenuante, por parte dos pesquisadores, de um modelo experimental que possa melhor caracterizar uma patologia täo importante para o ser humano como a hipertensäo essencial. Dentre os modelos genéticos de hipertensäo säo analisados os ratos com hipertensäo espontânea (SHR) e a cepa de ratos sensíveis à ingestäo de sódio (Dahl). Entre os modelos de hipertensäo neurogênica säo discutidos aqueles que envolvem a lesäo do núcleo do trato solitário (NTS), e o da deaferentaçäo sino-aórtica, associada, ou näo, à desnervaçäo das aferências cardiopulmonares. Entre as hipertensöes renais foram destacadas: a renovascular que decorre da oclusäo parcial da artéria renal; a renopriva, como o próprio nome indica; a perinefrítica que decorre da induçäo de fibrose renal pelo envolvimento do rim com um abrasivo contido por um tecido; e liberaçäo do pedículo renal após algumas horas de oclusäo total. O modelo de constriçäo (parcial ou total) da aorta abdominal examina os fatores mecânico e heurohumorais na elevaçäo da pressäo arterial. Um modelo descrito mais recentemente, que é examinado, é o do bloqueio da formaçäo de óxido nítrico (NO) com o L-NAME. E, finalmente, é apresentado o modelo de hipertensäo induzida pelo tratamento com deoxicorticosterona associado à ingestäo alta de sódio.
Descritores: Desoxicorticosterona/uso terapêutico
Hipertensão/genética
Hipertensão Renal
Óxido Nítrico
-Ratos Endogâmicos Dahl
Limites: Humanos
Animais
Tipo de Publ: Revisão
Responsável: BR26.1 - Biblioteca Central


  9 / 21 LILACS  
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Cabral, A. M
Mauad, H
Vasquez, E. C
Texto completo
Id: lil-212426
Autor: Cabral, A. M; Silva, I. F; Gardioli, C. R; Mauad, H; Vasquez, E. C.
Título: Diverse effects of renal denervation on ventricular hypertrophy and blood pressure in DOCA-salt hypertensive rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;31(4):587-90, Apr. 1998. tab, graf.
Idioma: en.
Resumo: Cardiac hypertrophy that accompanies hypertension seems to be a phenomenon of multifactorial origin whose development does not seem to depend on an increased pressure load alone, but also on local growth factores and cardioadrenergic activity. The aim of the present study was to determine if sympathetic renal denervation and its effects on arterial pressure level can prevent cardiac hypertrophy and if it can also delay the onset and attenuate the severity of deoxycorticosterone acetate (DOCA)-salt hypertension. DOCA-salt treatment was initiated in rats seven days after uninephrectomy and contralateral renal denervation or sham renal denervation. DOCA (15 mg/kg, sc) or vehicle (soybean oil, 0.25 ml per animal) was administered twice a week for two weeks. Rats treated with DOCA or vehicle (control) were provided drinking water containing 1 percent NaCl and 0.03 percent KCl. At the end of the treatment period, mean arterial pressure (MAP) and heart rate measurements were made in conscious animals. Under ether anesthesia, the heart was removed and the right and left ventricles (including the septum) were separated and weighed. DOCA-salt treatment produced a significant increase in left ventricular weight/body weight (LVW/BW) ratio (2.44 + 0.09 mg/g) and right ventricular weight/body weight (RVW/BW) ratio (0.53 + 0.01 mg/g) compared to control (1.92 + 0.04 and 0.48 + 0.01 mg/g, respectively) rats. MAP was significantly higher (39 percent) in DOCA-salt rats. Renal denervation prevented (P>0.05) the development of hypertension in DOCA-salt rats but did not prevent the increase in LVW/BW (2.27 + 0.03 mg/g) and RVW/BW (0.52 + 0.01 mg/g). We have shown that the increase in arterial pressure level is not responsible for cardiac hypertrophy, which may be more related to other events associated with DOCA-salt hypertension, such as an increase in cardiac sympathetic activity.
Descritores: Pressão Sanguínea/efeitos dos fármacos
Cardiomegalia
Desoxicorticosterona/uso terapêutico
Rim/inervação
Rim/cirurgia
Cloreto de Sódio na Dieta
-Cardiomegalia/tratamento farmacológico
Cardiomegalia/etiologia
Frequência Cardíaca/efeitos dos fármacos
Tamanho do Órgão
Ratos Wistar
Limites: Ratos
Animais
Masculino
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-188436
Autor: Tostes, R. C. A; Wilde, D. W; Bendhack, L. M; Webb, R. C.
Título: The effects of cyclopiazonic acid on intracellular Ca2+ in aortic smooth muscle cells from DOCA-hypertensive rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;30(2):257-67, Feb. 1997. ilus, graf.
Idioma: en.
Projeto: National Institutes of Health; . American Health Association.
Resumo: We tested the hypothesis that cyclopiazonic acid (CPA), an inhibitor of the sarcoplasmic reticulum (SR) Ca2+ -ATPase, increases intracellular Ca2+ concentration ([Ca2+]i) in aortic myocytes and that the increase in [Ca2+]i is higher in aortic cells from deoxycorticosterone acetate (DOCA)-hypertensive rats. Male Sprague-Dawley rats, 250-300 g, underwent uninephrectomy, received a silastic implant containing DOCA (200 mg/kg) and had free access to water supplemented with 1.0 per cent NaCl and 0.2 per cent KCl. Control rats were also uninephrectomized, received normal tap water, but no implant. Intracellular Ca2+ measurements were performed in aortic myocytes isolated from normotensive (Systolic blood pressure = 120 + 3 mmHg; body weight = 478 ñ 7 g, N = 7) and DOCA-hypertensive rats (195 ñ 1O mmHg; 358 ñ 16 g, N = 7). The effects of CPA on resting [Ca2+]i and on caffeine-induced increase in [Ca2+]i after [Ca2+]i depletion and reloading were compared in aortic cells from DOCA and normotensive rats. The phasic increase in [Ca2+]i induced by 20 mM caffeine in Ca2+ -free buffer was significantly higher in DOCA aortic cells (329 ñ 36 nM, N = 5) compared to that in normotensive cells (249 ñ 16 nM, N = 7, P<0.05). CPA (3 muM) inhibited caffeine-induced increases in [Ca2+]i in both groups. When the cells were placed in normal buffer (1.6 mM Ca2+, loading period), after treatment with Ca2+ -free buffer (depletion period), an increase in [Ca2+]i was observed in DOCA aortic cells (45 ñ 11 nM, N = 5) while no changes were observed in normotensive cells. CPA (3 muM) potentiated the increase in [Ca2+]i (l22 ñ 3O nM, N = 5) observed in DOCA cells during the loading period while only a modest increase in [Ca2+]i, (23 ñ 10 nM, N = 5) was observed in normotensive cells. CPA-induced increase in [Ca2+]i did not occur in the absence of extracellular Ca2+ or in the presence of nifedipine. These data show that CPA induces Ca2+ influx in aorta from both normotensive and DOCA-hypertensive rats. However, the increase in [Ca2+]i is higher in DOCA aortic cells possibly due to an impairment in the mechanisms that control [Ca2+]i. The large increase in [Ca2+]i in response to caffeine in DOCA cells probably reflects a greater storage of Ca2+ in the SR.
Descritores: Cafeína/farmacologia
Cálcio/metabolismo
Desoxicorticosterona/farmacologia
Inibidores Enzimáticos/farmacologia
Hipertensão/induzido quimicamente
Indóis/farmacologia
Músculo Liso Vascular/efeitos dos fármacos
Nifedipino/farmacologia
-Transporte de Íons/efeitos dos fármacos
Ratos Sprague-Dawley
Limites: Ratos
Animais
Masculino
Tipo de Publ: Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Responsável: BR1.1 - BIREME



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